https://npdslinks.org/Nexus/SOLOMON?ef=1&lc=11&vf=1Dissociable neural responses in human reward systems.Reward is one of the most important influences shaping behavior. Single-unit recording and lesion studies in experimental animals have implicated a number of regions in response to reinforcing stimuli, in particular regions of the extended limbic system and the ventral striatum. In this experiment, functional neuroimaging was used to assess neural response within human reward systems under different psychological contexts. Nine healthy volunteers were scanned using functional magnetic resonance imaging during the performance of a gambling task with financial rewards and penalties. We demonstrated neural sensitivity of midbrain and ventral striatal regions to financial rewards and hippocampal sensitivity to financial penalties. Furthermore, we show that neural responses in globus pallidus, thalamus, and subgenual cingulate were specific to high reward levels occurring in the context of increasing reward. Responses to both reward level in the context of increasing reward and penalty level in the context of incrElliott2000https://npds.brainwatch.net/nexus/solomon/elliott2000Brain Mapping; Brain, anatomy /\&/ histology/physiology; Emotions, physiology; Humans; Magnetic Resonance Imaging; Motivation; Neuropsychological Tests; Psychomotor Performance, physiology; Reward2023-12-17T14:25:27Z2023-12-17T14:25:28Zhttps://npds.npdslinks.net/nexus/npds-root/solomonhttps://npds.npdslinks.net/nexus/npds-root/solomonhttps://npds.npdslinks.net/nexus/npds-root/solomonhttps://npds.npdslinks.net/nexus/npds-root/bha-scribe@{ Abstract=[Reward is one of the most important influences shaping behavior. Single-unit recording and lesion studies in experimental animals have implicated a number of regions in response to reinforcing stimuli, in particular regions of the extended limbic system and the ventral striatum. In this experiment, functional neuroimaging was used to assess neural response within human reward systems under different psychological contexts. Nine healthy volunteers were scanned using functional magnetic resonance imaging during the performance of a gambling task with financial rewards and penalties. We demonstrated neural sensitivity of midbrain and ventral striatal regions to financial rewards and hippocampal sensitivity to financial penalties. Furthermore, we show that neural responses in globus pallidus, thalamus, and subgenual cingulate were specific to high reward levels occurring in the context of increasing reward. Responses to both reward level in the context of increasing reward and penalty level in the context of increasing penalty were seen in caudate, insula, and ventral prefrontal cortex. These results demonstrate dissociable neural responses to rewards and penalties that are dependent on the psychological context in which they are experienced.], AbstractParsed=[Reward is one of the most important influences shaping behavior. Single-unit recording and lesion studies in experimental animals have implicated a number of regions in response to reinforcing stimuli, in particular regions of the extended limbic system and the ventral striatum. In this experiment, functional neuroimaging was used to assess neural response within human reward systems under different psychological contexts. Nine healthy volunteers were scanned using functional magnetic resonance imaging during the performance of a gambling task with financial rewards and penalties. We demonstrated neural sensitivity of midbrain and ventral striatal regions to financial rewards and hippocampal sensitivity to financial penalties. Furthermore, we show that neural responses in globus pallidus, thalamus, and subgenual cingulate were specific to high reward levels occurring in the context of increasing reward. Responses to both reward level in the context of increasing reward and penalty level in the context of increasing penalty were seen in caudate, insula, and ventral prefrontal cortex. These results demonstrate dissociable neural responses to rewards and penalties that are dependent on the psychological context in which they are experienced.], Author=[Elliott, R. and Friston, K. J. and Dolan, R. J.], CitationKey=[Elliott2000], Institution=[Wellcome Department of Cognitive Neurology, Institute of Neurology, London WC1N 3BG, United Kingdom. rebecca.elliott@man.ac.uk], Journal=[J Neurosci], Keywords=[Brain Mapping; Brain, anatomy /\&/ histology/physiology; Emotions, physiology; Humans; Magnetic Resonance Imaging; Motivation; Neuropsychological Tests; Psychomotor Performance, physiology; Reward], KeywordsParsed=[Brain Mapping; Brain, anatomy /\&/ histology/physiology; Emotions, physiology; Humans; Magnetic Resonance Imaging; Motivation; Neuropsychological Tests; Psychomotor Performance, physiology; Reward], Language=[eng], ModificationDate=[2021-12-03T12:29:21], Month=[8], Number=[16], Pages=[6159--6165], PMID=[10934265], ReferenceType=[Article], Title=[Dissociable neural responses in human reward systems.], TitleParsed=[Dissociable neural responses in human reward systems.], Volume=[20], Year=[2000], }@Public NPDS record with handle 'BE783BAC8' registered in 'SOLOMON ACMS' service by user with alias '' on 12/17/2023 6:25:27 AM.Management impact of FDG-PET in dementia: results from a tertiary center memory clinic.Elias2014https://npds.brainwatch.net/nexus/solomon/elias20142023-12-17T14:24:57Z2023-12-17T14:24:57Zhttps://npds.npdslinks.net/nexus/npds-root/solomonhttps://npds.npdslinks.net/nexus/npds-root/solomonhttps://npds.npdslinks.net/nexus/npds-root/solomonhttps://npds.npdslinks.net/nexus/npds-root/bha-scribe@{ AbstractParsed=[], Author=[Elias, Alby and Woodward, Michael and Rowe, Christopher C.], CitationKey=[Elias2014], DOI=[10.3233/JAD-132729], Institution=[Department of Nuclear Medicine and Centre for PET, Austin Health, The University of Melbourne, VIC, Australia.], Journal=[J Alzheimers Dis], KeywordsParsed=[], Language=[eng], Number=[3], Owner=[ctaswell], Pages=[885--892], PMID=[24961944], ReferenceType=[Article], TimeStamp=[2014.11.24], Title=[Management impact of FDG-PET in dementia: results from a tertiary center memory clinic.], TitleParsed=[Management impact of FDG-PET in dementia: results from a tertiary center memory clinic.], URL=[http://dx.doi.org/10.3233/JAD-132729], Volume=[42], Year=[2014], }@Public NPDS record with handle 'H425EC866' registered in 'SOLOMON ACMS' service by user with alias '' on 12/17/2023 6:24:57 AM.Quantitative SPECT leads to improved performance in discrimination tasks related to prodromal Alzheimer's disease.We investigated the impact of the quantitation and reconstruction protocol on clinical tasks. The performance of standard clinical reconstruction procedures in discrimination tasks related to the diagnosis of prodromal Alzheimer's disease (AD) was compared with the performance of a quantitative approach incorporating improved corrections for scatter, attenuation, intrinsic spatial resolution, and distance-dependent spatial resolution.Seventeen normal controls (normal group), 56 subjects who did not have dementia, who did have memory problems, but who did not develop AD within 5 y of follow-up (questionable group), and 27 subjects who did not have dementia, who did have memory problems, and who did develop AD over the follow-up period (converter group) were considered in this study. (99m)Tc-hexamethylpropyleneamine oxime SPECT and MRI studies were performed for each subject at baseline. The standard quantitation protocol (STD), routinely used in our clinic, consisted of Compton window scatter correction followElFakhri2004https://npds.brainwatch.net/nexus/solomon/elfakhri2004Aged; Alzheimer Disease, pathology/radionuclide imaging; Brain, pathology/radionuclide imaging; Dementia, pathology/radionuclide imaging; Humans; Image Processing, Computer-Assisted; Magnetic Resonance Imaging, methods; Technetium Tc 99m Exametazime, diagn2023-12-17T14:24:26Z2023-12-17T14:24:27Zhttps://npds.npdslinks.net/nexus/npds-root/solomonhttps://npds.npdslinks.net/nexus/npds-root/solomonhttps://npds.npdslinks.net/nexus/npds-root/solomonhttps://npds.npdslinks.net/nexus/npds-root/bha-scribe@{ Abstract=[We investigated the impact of the quantitation and reconstruction protocol on clinical tasks. The performance of standard clinical reconstruction procedures in discrimination tasks related to the diagnosis of prodromal Alzheimer's disease (AD) was compared with the performance of a quantitative approach incorporating improved corrections for scatter, attenuation, intrinsic spatial resolution, and distance-dependent spatial resolution.Seventeen normal controls (normal group), 56 subjects who did not have dementia, who did have memory problems, but who did not develop AD within 5 y of follow-up (questionable group), and 27 subjects who did not have dementia, who did have memory problems, and who did develop AD over the follow-up period (converter group) were considered in this study. (99m)Tc-hexamethylpropyleneamine oxime SPECT and MRI studies were performed for each subject at baseline. The standard quantitation protocol (STD), routinely used in our clinic, consisted of Compton window scatter correction followed by filtered backprojection with attenuation correction using a uniform attenuation map. In the improved quantitative approach (QUAN), projections were corrected for scatter by use of a general spectral method and reconstructed by use of ordered-subset(s) expectation maximization, incorporating corrections for collimator response and attenuation using both a uniform attenuation map (QUANunif) and a nonuniform attenuation map (QUANnonunif). Mean SPECT activity concentration and MRI volume were estimated for 7 structures: rostral anterior cingulate gyrus, caudal anterior cingulate gyrus, posterior cingulate gyrus, hippocampus, basal forebrain, amygdala, and the banks of the superior temporal sulcus. Data were analyzed by pairwise discriminant analysis, and performance in binary group discrimination was measured by correlated receiver-operating-characteristic analysis.The use of QUANnonunif yielded a small but systematic improvement in discrimination accuracy for normal versus converter groups (accuracy or area under the receiver-operating-characteristic curve [Az], AbstractParsed=[We investigated the impact of the quantitation and reconstruction protocol on clinical tasks. The performance of standard clinical reconstruction procedures in discrimination tasks related to the diagnosis of prodromal Alzheimer's disease (AD) was compared with the performance of a quantitative approach incorporating improved corrections for scatter, attenuation, intrinsic spatial resolution, and distance-dependent spatial resolution.Seventeen normal controls (normal group), 56 subjects who did not have dementia, who did have memory problems, but who did not develop AD within 5 y of follow-up (questionable group), and 27 subjects who did not have dementia, who did have memory problems, and who did develop AD over the follow-up period (converter group) were considered in this study. (99m)Tc-hexamethylpropyleneamine oxime SPECT and MRI studies were performed for each subject at baseline. The standard quantitation protocol (STD), routinely used in our clinic, consisted of Compton window scatter correction followed by filtered backprojection with attenuation correction using a uniform attenuation map. In the improved quantitative approach (QUAN), projections were corrected for scatter by use of a general spectral method and reconstructed by use of ordered-subset(s) expectation maximization, incorporating corrections for collimator response and attenuation using both a uniform attenuation map (QUANunif) and a nonuniform attenuation map (QUANnonunif). Mean SPECT activity concentration and MRI volume were estimated for 7 structures: rostral anterior cingulate gyrus, caudal anterior cingulate gyrus, posterior cingulate gyrus, hippocampus, basal forebrain, amygdala, and the banks of the superior temporal sulcus. Data were analyzed by pairwise discriminant analysis, and performance in binary group discrimination was measured by correlated receiver-operating-characteristic analysis.The use of QUANnonunif yielded a small but systematic improvement in discrimination accuracy for normal versus converter groups (accuracy or area under the receiver-operating-characteristic curve [Az], Author=[{El Fakhri], CitationKey=[ElFakhri2004], Institution=[Department of Radiology, Harvard Medical School, Boston, Massachusetts 02115, USA. elfakhri@bwh.harvard.edu], Journal=[J Nucl Med], Keywords=[Aged; Alzheimer Disease, pathology/radionuclide imaging; Brain, pathology/radionuclide imaging; Dementia, pathology/radionuclide imaging; Humans; Image Processing, Computer-Assisted; Magnetic Resonance Imaging, methods; Technetium Tc 99m Exametazime, diagnostic use; Tomography, Emission-Computed, Single-Photon, methods], KeywordsParsed=[Aged; Alzheimer Disease, pathology/radionuclide imaging; Brain, pathology/radionuclide imaging; Dementia, pathology/radionuclide imaging; Humans; Image Processing, Computer-Assisted; Magnetic Resonance Imaging, methods; Technetium Tc 99m Exametazime, diagnostic use; Tomography, Emission-Computed, Single-Photon, methods], Language=[eng], ModificationDate=[2021-12-03T12:29:21], Month=[12], Number=[12], Owner=[ctaswell], Pages=[2026--2031], PMID=[15585477], ReferenceType=[Article], TimeStamp=[2014.11.30], Title=[Quantitative SPECT leads to improved performance in discrimination tasks related to prodromal Alzheimer's disease.], TitleParsed=[Quantitative SPECT leads to improved performance in discrimination tasks related to prodromal Alzheimer's disease.], Volume=[45], Year=[2004], }@Public NPDS record with handle 'L8F0C04EB' registered in 'SOLOMON ACMS' service by user with alias '' on 12/17/2023 6:24:26 AM.MRI-guided SPECT perfusion measures and volumetric MRI in prodromal Alzheimer disease.To identify group differences in the prodromal phase of Alzheimer disease (AD) using quantitative single-photon emission computed tomography (SPECT) perfusion and magnetic resonance imaging (MRI) volume measures within specific volumes of interest.Gerontology research unit.There were 17 healthy controls, 56 nondemented patients with memory problems who did not develop AD during 3 to 5 years of follow-up (questionables), and 27 nondemented patients with memory problems who developed AD during follow-up (converters).A Tc 99m hexamethylpropyleneamine oxime SPECT study and an MRI were performed in each participant at baseline. Mean SPECT activity concentration and MRI volume were estimated within 9 structures: rostral anterior cingulate, caudal anterior cingulate, posterior cingulate, hippocampus, entorhinal cortex, basal forebrain, temporal horn, amygdala, and the banks of the superior temporal sulcus. Data were analyzed using overall and pairwise discriminant analysis, and performance in pairwise group discrimiElFakhri2003https://npds.brainwatch.net/nexus/solomon/elfakhri2003Aged; Alzheimer Disease, pathology/radiography/radionuclide imaging; Brain, pathology; Humans; Magnetic Resonance Imaging; Memory Disorders, pathology/radiography/radionuclide imaging; Predictive Value of Tests; Technetium Tc 99m Exametazime, diagnostic us2023-12-17T14:23:56Z2023-12-17T14:23:56Zhttps://npds.npdslinks.net/nexus/npds-root/solomonhttps://npds.npdslinks.net/nexus/npds-root/solomonhttps://npds.npdslinks.net/nexus/npds-root/solomonhttps://npds.npdslinks.net/nexus/npds-root/bha-scribe@{ Abstract=[To identify group differences in the prodromal phase of Alzheimer disease (AD) using quantitative single-photon emission computed tomography (SPECT) perfusion and magnetic resonance imaging (MRI) volume measures within specific volumes of interest.Gerontology research unit.There were 17 healthy controls, 56 nondemented patients with memory problems who did not develop AD during 3 to 5 years of follow-up (questionables), and 27 nondemented patients with memory problems who developed AD during follow-up (converters).A Tc 99m hexamethylpropyleneamine oxime SPECT study and an MRI were performed in each participant at baseline. Mean SPECT activity concentration and MRI volume were estimated within 9 structures: rostral anterior cingulate, caudal anterior cingulate, posterior cingulate, hippocampus, entorhinal cortex, basal forebrain, temporal horn, amygdala, and the banks of the superior temporal sulcus. Data were analyzed using overall and pairwise discriminant analysis, and performance in pairwise group discrimination was measured using correlated receiver operating characteristic curve analysis.The overall (3-group) discriminant function was significant for SPECT (F test, P<.001) and MRI (F test, P<.0001). For the SPECT analysis, the ranking of structures for discriminating among the 3 groups was, in order of decreasing discriminating power, caudal anterior cingulate, temporal horn, superior temporal sulcus, entorhinal cortex, hippocampus, rostral anterior cingulate, amygdala, basal forebrain, and posterior cingulate. For the MRI analysis, this ranking was entorhinal cortex, superior temporal sulcus, temporal horn, hippocampus, amygdala, caudal anterior cingulate, rostral anterior cingulate, basal forebrain, and posterior cingulate. Combining the 2 modalities yielded significantly better discrimination performance than did either alone. Furthermore, the correlation between SPECT and MRI measures was low.Measures of structure activity concentration and volume carry independent information; both reveal group differences in prodromal AD.], AbstractParsed=[To identify group differences in the prodromal phase of Alzheimer disease (AD) using quantitative single-photon emission computed tomography (SPECT) perfusion and magnetic resonance imaging (MRI) volume measures within specific volumes of interest.Gerontology research unit.There were 17 healthy controls, 56 nondemented patients with memory problems who did not develop AD during 3 to 5 years of follow-up (questionables), and 27 nondemented patients with memory problems who developed AD during follow-up (converters).A Tc 99m hexamethylpropyleneamine oxime SPECT study and an MRI were performed in each participant at baseline. Mean SPECT activity concentration and MRI volume were estimated within 9 structures: rostral anterior cingulate, caudal anterior cingulate, posterior cingulate, hippocampus, entorhinal cortex, basal forebrain, temporal horn, amygdala, and the banks of the superior temporal sulcus. Data were analyzed using overall and pairwise discriminant analysis, and performance in pairwise group discrimination was measured using correlated receiver operating characteristic curve analysis.The overall (3-group) discriminant function was significant for SPECT (F test, P<.001) and MRI (F test, P<.0001). For the SPECT analysis, the ranking of structures for discriminating among the 3 groups was, in order of decreasing discriminating power, caudal anterior cingulate, temporal horn, superior temporal sulcus, entorhinal cortex, hippocampus, rostral anterior cingulate, amygdala, basal forebrain, and posterior cingulate. For the MRI analysis, this ranking was entorhinal cortex, superior temporal sulcus, temporal horn, hippocampus, amygdala, caudal anterior cingulate, rostral anterior cingulate, basal forebrain, and posterior cingulate. Combining the 2 modalities yielded significantly better discrimination performance than did either alone. Furthermore, the correlation between SPECT and MRI measures was low.Measures of structure activity concentration and volume carry independent information; both reveal group differences in prodromal AD.], Author=[{El Fakhri], CitationKey=[ElFakhri2003], DOI=[10.1001/archneur.60.8.1066], Institution=[Department of Radiology, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115, USA. elfakhri@bwh.harvard.edu], Journal=[Arch Neurol], Keywords=[Aged; Alzheimer Disease, pathology/radiography/radionuclide imaging; Brain, pathology; Humans; Magnetic Resonance Imaging; Memory Disorders, pathology/radiography/radionuclide imaging; Predictive Value of Tests; Technetium Tc 99m Exametazime, diagnostic use; Tomography, Emission-Computed, Single-Photon], KeywordsParsed=[Aged; Alzheimer Disease, pathology/radiography/radionuclide imaging; Brain, pathology; Humans; Magnetic Resonance Imaging; Memory Disorders, pathology/radiography/radionuclide imaging; Predictive Value of Tests; Technetium Tc 99m Exametazime, diagnostic use; Tomography, Emission-Computed, Single-Photon], Language=[eng], ModificationDate=[2021-12-03T12:29:21], Month=[8], Number=[8], Owner=[ctaswell], Pages=[1066--1072], PMID=[12925361], ReferenceType=[Article], TimeStamp=[2014.11.30], Title=[MRI-guided SPECT perfusion measures and volumetric MRI in prodromal Alzheimer disease.], TitleParsed=[MRI-guided SPECT perfusion measures and volumetric MRI in prodromal Alzheimer disease.], URL=[http://dx.doi.org/10.1001/archneur.60.8.1066], Volume=[60], Year=[2003], }@Public NPDS record with handle 'O19F0CDBA' registered in 'SOLOMON ACMS' service by user with alias '' on 12/17/2023 6:23:56 AM.Spatial and temporal variability in VOC levels within a commercial retail building.A study was performed to characterize the concentration of dozens of volatile organic compounds (VOCs) at 10 locations within a single large building and track these concentrations over a 2-year period. The study was performed at a shopping center (strip mall) in New Jersey. A total of 130 indoor air samples were collected from 10 retail stores within the shopping center and analyzed for 60 VOCs by US EPA Method TO-15. Indoor concentrations of up to 55,100 microg/m(3) were measured for individual VOCs. The indoor/outdoor ratio (I/O) was as high as 1500 for acetone and exceeded 100 at times for various compounds, indicating that significant indoor air sources were present. A large degree of spatial variability was observed between stores within the building, with concentrations varying by three to four orders of magnitude for some compounds. The spatial variability was dependent on the proximity of the sampling locations to the indoor sources. A large degree of temporal variability also was observed for compouEklund2008https://npds.brainwatch.net/nexus/solomon/eklund2008Air Pollutants, Occupational, analysis; Air Pollution, Indoor, analysis; Construction Materials, adverse effects/analysis; Environmental Monitoring; Humans; Public Facilities; Risk Assessment; Ventilation; Volatile Organic Compounds, analysis; Volatilizati2023-12-17T14:23:25Z2023-12-17T14:23:26Zhttps://npds.npdslinks.net/nexus/npds-root/solomonhttps://npds.npdslinks.net/nexus/npds-root/solomonhttps://npds.npdslinks.net/nexus/npds-root/solomonhttps://npds.npdslinks.net/nexus/npds-root/bha-scribe@{ Abstract=[A study was performed to characterize the concentration of dozens of volatile organic compounds (VOCs) at 10 locations within a single large building and track these concentrations over a 2-year period. The study was performed at a shopping center (strip mall) in New Jersey. A total of 130 indoor air samples were collected from 10 retail stores within the shopping center and analyzed for 60 VOCs by US EPA Method TO-15. Indoor concentrations of up to 55,100 microg/m(3) were measured for individual VOCs. The indoor/outdoor ratio (I/O) was as high as 1500 for acetone and exceeded 100 at times for various compounds, indicating that significant indoor air sources were present. A large degree of spatial variability was observed between stores within the building, with concentrations varying by three to four orders of magnitude for some compounds. The spatial variability was dependent on the proximity of the sampling locations to the indoor sources. A large degree of temporal variability also was observed for compounds emitted from indoor sources, but the temporal variability generally did not exceed two standard deviations (sigma). For compounds not emitted from indoor sources at significant rates, both the spatial and temporal variability tended to range within an order of magnitude at each location.Many cross-sectional studies have been published where the levels of volatile organic compounds (VOCs) were measured in indoor air at one or two locations for houses or offices. This study provides longitudinal data for a commercial retail building and also addresses spatial variability within the building. The data suggest that spatial and temporal variability are important considerations for compounds emitted from indoor sources. Elevated concentrations were found in retail spaces with no apparent emission sources due to their proximity to other retail spaces with emission sources.], AbstractParsed=[A study was performed to characterize the concentration of dozens of volatile organic compounds (VOCs) at 10 locations within a single large building and track these concentrations over a 2-year period. The study was performed at a shopping center (strip mall) in New Jersey. A total of 130 indoor air samples were collected from 10 retail stores within the shopping center and analyzed for 60 VOCs by US EPA Method TO-15. Indoor concentrations of up to 55,100 microg/m(3) were measured for individual VOCs. The indoor/outdoor ratio (I/O) was as high as 1500 for acetone and exceeded 100 at times for various compounds, indicating that significant indoor air sources were present. A large degree of spatial variability was observed between stores within the building, with concentrations varying by three to four orders of magnitude for some compounds. The spatial variability was dependent on the proximity of the sampling locations to the indoor sources. A large degree of temporal variability also was observed for compounds emitted from indoor sources, but the temporal variability generally did not exceed two standard deviations (sigma). For compounds not emitted from indoor sources at significant rates, both the spatial and temporal variability tended to range within an order of magnitude at each location.Many cross-sectional studies have been published where the levels of volatile organic compounds (VOCs) were measured in indoor air at one or two locations for houses or offices. This study provides longitudinal data for a commercial retail building and also addresses spatial variability within the building. The data suggest that spatial and temporal variability are important considerations for compounds emitted from indoor sources. Elevated concentrations were found in retail spaces with no apparent emission sources due to their proximity to other retail spaces with emission sources.], Author=[Eklund, B. M. and Burkes, S. and Morris, P. and Mosconi, L.], CitationKey=[Eklund2008], DOI=[10.1111/j.1600-0668.2008.00537.x], Institution=[URS Corporation, Austin, TX 78729, USA. diogobolster@gmail.com], Journal=[Indoor Air], Keywords=[Air Pollutants, Occupational, analysis; Air Pollution, Indoor, analysis; Construction Materials, adverse effects/analysis; Environmental Monitoring; Humans; Public Facilities; Risk Assessment; Ventilation; Volatile Organic Compounds, analysis; Volatilization; Workplace], KeywordsParsed=[Air Pollutants, Occupational, analysis; Air Pollution, Indoor, analysis; Construction Materials, adverse effects/analysis; Environmental Monitoring; Humans; Public Facilities; Risk Assessment; Ventilation; Volatile Organic Compounds, analysis; Volatilization; Workplace], Language=[eng], ModificationDate=[2021-12-03T12:29:21], Month=[10], Number=[5], Owner=[ctaswell], Pages=[365--374], PMID=[18636973], ReferenceType=[Article], TimeStamp=[2014.11.25], Title=[Spatial and temporal variability in VOC levels within a commercial retail building.], TitleParsed=[Spatial and temporal variability in VOC levels within a commercial retail building.], URL=[http://dx.doi.org/10.1111/j.1600-0668.2008.00537.x], Volume=[18], Year=[2008], }@Public NPDS record with handle 'KC3E68634' registered in 'SOLOMON ACMS' service by user with alias '' on 12/17/2023 6:23:25 AM.Preliminary evidence that negative symptom severity relates to multilocus genetic profile for dopamine signaling capacity and D2 receptor binding in healthy controls and in schizophrenia.Deficits in central, subcortical dopamine (DA) signaling may underlie negative symptom severity, particularly anhedonia, in healthy individuals and in schizophrenia. To investigate these relationships, we assessed negative symptoms with the Schedule for the Assessment of Negative Symptoms and the Brief Negative Symptom Scale (BNSS) and self-reported anhedonia with the Scales for Physical and Social Anhedonia (SPSA), Temporal Experience of Pleasure Scale, and Snaith-Hamilton Pleasure Scale in 36 healthy controls (HC), 27 siblings (SIB) of individuals with schizophrenia, and 66 individuals with schizophrenia or schizoaffective disorder (SCZ). A subset of participants (N?=?124) were genotyped for DA-related polymorphisms in genes for DRD4, DRD2/ANKK1, DAT1, and COMT, which were used to construct biologically-informed multi-locus genetic profile (MGP) scores reflective of subcortical dopaminergic signaling. DA receptor type 2 (D2R) binding was assessed among a second subset of participants (N?=?23) using PET scanEisenstein2017https://npds.brainwatch.net/nexus/solomon/eisenstein2017Anhedonia; Dopamine; Genetic profile; Negative symptoms; PET; Schizophrenia2023-12-17T14:22:55Z2023-12-17T14:22:55Zhttps://npds.npdslinks.net/nexus/npds-root/solomonhttps://npds.npdslinks.net/nexus/npds-root/solomonhttps://npds.npdslinks.net/nexus/npds-root/solomonhttps://npds.npdslinks.net/nexus/npds-root/bha-scribe@{ Abstract=[Deficits in central, subcortical dopamine (DA) signaling may underlie negative symptom severity, particularly anhedonia, in healthy individuals and in schizophrenia. To investigate these relationships, we assessed negative symptoms with the Schedule for the Assessment of Negative Symptoms and the Brief Negative Symptom Scale (BNSS) and self-reported anhedonia with the Scales for Physical and Social Anhedonia (SPSA), Temporal Experience of Pleasure Scale, and Snaith-Hamilton Pleasure Scale in 36 healthy controls (HC), 27 siblings (SIB) of individuals with schizophrenia, and 66 individuals with schizophrenia or schizoaffective disorder (SCZ). A subset of participants (N?=?124) were genotyped for DA-related polymorphisms in genes for DRD4, DRD2/ANKK1, DAT1, and COMT, which were used to construct biologically-informed multi-locus genetic profile (MGP) scores reflective of subcortical dopaminergic signaling. DA receptor type 2 (D2R) binding was assessed among a second subset of participants (N?=?23) using PET scans with the D2R-selective, non-displaceable radioligand (N-[(11)C]methyl)benperidol. Higher MGP scores, reflecting elevated subcortical dopaminergic signaling capacity, were associated with less negative symptom severity, as measured by the BNSS, across all participants. In addition, higher striatal D2R binding was associated with less physical and social anhedonia, as measured by the SPSA, across HC, SIB, and SCZ. The current preliminary findings support the hypothesis that subcortical DA function may contribute to negative symptom severity and self-reported anhedonia, independent of diagnostic status.], AbstractParsed=[Deficits in central, subcortical dopamine (DA) signaling may underlie negative symptom severity, particularly anhedonia, in healthy individuals and in schizophrenia. To investigate these relationships, we assessed negative symptoms with the Schedule for the Assessment of Negative Symptoms and the Brief Negative Symptom Scale (BNSS) and self-reported anhedonia with the Scales for Physical and Social Anhedonia (SPSA), Temporal Experience of Pleasure Scale, and Snaith-Hamilton Pleasure Scale in 36 healthy controls (HC), 27 siblings (SIB) of individuals with schizophrenia, and 66 individuals with schizophrenia or schizoaffective disorder (SCZ). A subset of participants (N?=?124) were genotyped for DA-related polymorphisms in genes for DRD4, DRD2/ANKK1, DAT1, and COMT, which were used to construct biologically-informed multi-locus genetic profile (MGP) scores reflective of subcortical dopaminergic signaling. DA receptor type 2 (D2R) binding was assessed among a second subset of participants (N?=?23) using PET scans with the D2R-selective, non-displaceable radioligand (N-[(11)C]methyl)benperidol. Higher MGP scores, reflecting elevated subcortical dopaminergic signaling capacity, were associated with less negative symptom severity, as measured by the BNSS, across all participants. In addition, higher striatal D2R binding was associated with less physical and social anhedonia, as measured by the SPSA, across HC, SIB, and SCZ. The current preliminary findings support the hypothesis that subcortical DA function may contribute to negative symptom severity and self-reported anhedonia, independent of diagnostic status.], Author=[Eisenstein, Sarah A and Bogdan, Ryan and Chen, Ling and Moerlein, Stephen M and Black, Kevin J and Perlmutter, Joel S and Hershey, Tamara and Barch, Deanna M], CitationKey=[Eisenstein2017], Country=[England], Created=[2016-11-25], DOI=[10.1016/j.jpsychires.2016.11.007], ISSN=[1879-1379], Journal=[Journal of psychiatric research], Keywords=[Anhedonia; Dopamine; Genetic profile; Negative symptoms; PET; Schizophrenia], KeywordsParsed=[Anhedonia; Dopamine; Genetic profile; Negative symptoms; PET; Schizophrenia], MID=[NIHMS831878], Month=[3], Owner=[bhavius], Pages=[9--17], PMID=[27886638], PubModel=[Print-Electronic], PubStatus=[ppublish], ReferenceType=[Article], Revised=[2017-02-20], TimeStamp=[2017-03-05], Title=[Preliminary evidence that negative symptom severity relates to multilocus genetic profile for dopamine signaling capacity and D2 receptor binding in healthy controls and in schizophrenia.], TitleParsed=[Preliminary evidence that negative symptom severity relates to multilocus genetic profile for dopamine signaling capacity and D2 receptor binding in healthy controls and in schizophrenia.], Volume=[86], Year=[2017], }@Public NPDS record with handle 'J13851849' registered in 'SOLOMON ACMS' service by user with alias '' on 12/17/2023 6:22:55 AM.Correction: Insulin, Central Dopamine D2 Receptors, and Monetary Reward Discounting in Obesity.Eisenstein2016ahttps://npds.brainwatch.net/nexus/solomon/eisenstein2016a2023-12-17T14:22:24Z2023-12-17T14:22:25Zhttps://npds.npdslinks.net/nexus/npds-root/solomonhttps://npds.npdslinks.net/nexus/npds-root/solomonhttps://npds.npdslinks.net/nexus/npds-root/solomonhttps://npds.npdslinks.net/nexus/npds-root/bha-scribe@{ AbstractParsed=[], Author=[Eisenstein, Sarah A and Gredysa, Danuta M and Antenor-Dorsey, Jo Ann and Green, Leonard and Arbel?ez, Ana Maria and Koller, Jonathan M and Black, Kevin J and Perlmutter, Joel S and Moerlein, Stephen M and Hershey, Tamara], CitationKey=[Eisenstein2016a], Country=[United States], Created=[2016-01-09], DOI=[10.1371/journal.pone.0147063], ISSN=[1932-6203], Issue=[1], Journal=[PloS one], KeywordsParsed=[], Owner=[bhavius], Pages=[e0147063], PMID=[26744894], PubModel=[Electronic-eCollection], PubStatus=[epublish], ReferenceType=[Article], Revised=[2017-02-20], TimeStamp=[2017-03-05], Title=[Correction: Insulin, Central Dopamine D2 Receptors, and Monetary Reward Discounting in Obesity.], TitleParsed=[Correction: Insulin, Central Dopamine D2 Receptors, and Monetary Reward Discounting in Obesity.], Volume=[11], Year=[2016], }@Public NPDS record with handle 'L4BAD33E6' registered in 'SOLOMON ACMS' service by user with alias '' on 12/17/2023 6:22:24 AM.Prediction of striatal D2 receptor binding by DRD2/ANKK1 TaqIA allele status.In humans, the A1 (T) allele of the dopamine (DA) D2 receptor/ankyrin repeat and kinase domain containing 1 (DRD2/ANKK1) TaqIA (rs1800497) single nucleotide polymorphism has been associated with reduced striatal DA D2/D3 receptor (D2/D3R) availability. However, radioligands used to estimate D2/D3R are displaceable by endogenous DA and are nonselective for D2R, leaving the relationship between TaqIA genotype and D2R specific binding uncertain. Using the positron emission tomography (PET) radioligand, (N-[(11) C]methyl)benperidol ([(11) C]NMB), which is highly selective for D2R over D3R and is not displaceable by endogenous DA, the current study examined whether DRD2/ANKK1 TaqIA genotype predicts D2R specific binding in two independent samples. Sample 1 (n?=?39) was composed of obese and nonobese adults; sample 2 (n?=?18) was composed of healthy controls, unmedicated individuals with schizophrenia, and siblings of individuals with schizophrenia. Across both samples, A1 allele carriers (A1+) had 5 to 12\% less sEisenstein2016https://npds.brainwatch.net/nexus/solomon/eisenstein2016PET; dopamine; rs18004972023-12-17T14:21:54Z2023-12-17T14:21:54Zhttps://npds.npdslinks.net/nexus/npds-root/solomonhttps://npds.npdslinks.net/nexus/npds-root/solomonhttps://npds.npdslinks.net/nexus/npds-root/solomonhttps://npds.npdslinks.net/nexus/npds-root/bha-scribe@{ Abstract=[In humans, the A1 (T) allele of the dopamine (DA) D2 receptor/ankyrin repeat and kinase domain containing 1 (DRD2/ANKK1) TaqIA (rs1800497) single nucleotide polymorphism has been associated with reduced striatal DA D2/D3 receptor (D2/D3R) availability. However, radioligands used to estimate D2/D3R are displaceable by endogenous DA and are nonselective for D2R, leaving the relationship between TaqIA genotype and D2R specific binding uncertain. Using the positron emission tomography (PET) radioligand, (N-[(11) C]methyl)benperidol ([(11) C]NMB), which is highly selective for D2R over D3R and is not displaceable by endogenous DA, the current study examined whether DRD2/ANKK1 TaqIA genotype predicts D2R specific binding in two independent samples. Sample 1 (n?=?39) was composed of obese and nonobese adults; sample 2 (n?=?18) was composed of healthy controls, unmedicated individuals with schizophrenia, and siblings of individuals with schizophrenia. Across both samples, A1 allele carriers (A1+) had 5 to 12\% less striatal D2R specific binding relative to individuals homozygous for the A2 allele (A1-), regardless of body mass index or diagnostic group. This reduction is comparable to previous PET studies of D2/D3R availability (10-14\%). The pooled effect size for the difference in total striatal D2R binding between A1+ and A1- was large (0.84). In summary, in line with studies using displaceable D2/D3R radioligands, our results indicate that DRD2/ANKK1 TaqIA allele status predicts striatal D2R specific binding as measured by D2R-selective [(11) C]NMB. These findings support the hypothesis that DRD2/ANKK1 TaqIA allele status may modify D2R, perhaps conferring risk for certain disease states.], AbstractParsed=[In humans, the A1 (T) allele of the dopamine (DA) D2 receptor/ankyrin repeat and kinase domain containing 1 (DRD2/ANKK1) TaqIA (rs1800497) single nucleotide polymorphism has been associated with reduced striatal DA D2/D3 receptor (D2/D3R) availability. However, radioligands used to estimate D2/D3R are displaceable by endogenous DA and are nonselective for D2R, leaving the relationship between TaqIA genotype and D2R specific binding uncertain. Using the positron emission tomography (PET) radioligand, (N-[(11) C]methyl)benperidol ([(11) C]NMB), which is highly selective for D2R over D3R and is not displaceable by endogenous DA, the current study examined whether DRD2/ANKK1 TaqIA genotype predicts D2R specific binding in two independent samples. Sample 1 (n?=?39) was composed of obese and nonobese adults; sample 2 (n?=?18) was composed of healthy controls, unmedicated individuals with schizophrenia, and siblings of individuals with schizophrenia. Across both samples, A1 allele carriers (A1+) had 5 to 12\% less striatal D2R specific binding relative to individuals homozygous for the A2 allele (A1-), regardless of body mass index or diagnostic group. This reduction is comparable to previous PET studies of D2/D3R availability (10-14\%). The pooled effect size for the difference in total striatal D2R binding between A1+ and A1- was large (0.84). In summary, in line with studies using displaceable D2/D3R radioligands, our results indicate that DRD2/ANKK1 TaqIA allele status predicts striatal D2R specific binding as measured by D2R-selective [(11) C]NMB. These findings support the hypothesis that DRD2/ANKK1 TaqIA allele status may modify D2R, perhaps conferring risk for certain disease states.], Author=[Eisenstein, Sarah A and Bogdan, Ryan and Love-Gregory, Latisha and Corral-Fr?as, Nadia S and Koller, Jonathan M and Black, Kevin J and Moerlein, Stephen M and Perlmutter, Joel S and Barch, Deanna M and Hershey, Tamara], CitationKey=[Eisenstein2016], Country=[United States], Created=[2016-08-09], DOI=[10.1002/syn.21916], ISSN=[1098-2396], Issue=[10], Journal=[Synapse (New York, N.Y.)], Keywords=[PET; dopamine; rs1800497], KeywordsParsed=[PET; dopamine; rs1800497], MID=[NIHMS791575], Month=[10], Owner=[bhavius], Pages=[418--431], PMID=[27241797], PubModel=[Print-Electronic], PubStatus=[ppublish], ReferenceType=[Article], Revised=[2017-02-20], TimeStamp=[2017-03-05], Title=[Prediction of striatal D2 receptor binding by DRD2/ANKK1 TaqIA allele status.], TitleParsed=[Prediction of striatal D2 receptor binding by DRD2/ANKK1 TaqIA allele status.], Volume=[70], Year=[2016], }@Public NPDS record with handle 'SCF6C09B6' registered in 'SOLOMON ACMS' service by user with alias '' on 12/17/2023 6:21:54 AM.Advances in PET Imaging of Degenerative, Cerebrovascular, and Traumatic Causes of Dementia.In this review we present the most recent advances in nuclear medicine imaging as a diagnostic and management tool for dementia. The clinical diagnosis of dementia syndromes can be challenging for physicians, particularly in the early stages of disease. Given the growing number of individuals affected by dementia, early and accurate diagnosis can lead to improved clinical management of patients. Although tests are available for exclusion of certain causes of cognitive impairment, the results rarely allow the clinician to make a definitive diagnosis. For this reason, information obtained from imaging ("imaging biomarkers") is playing an increasingly important role in the workup of patients with suspected dementia. Imaging biomarkers also provide indispensable tools for clinical and preclinical studies of dementing illnesses to elucidate their pathophysiology and to develop better therapies. A wide range of imaging has been used to diagnose and investigate neurodegenerative disorders including structural, cerebEisenmenger2016https://npds.brainwatch.net/nexus/solomon/eisenmenger20162023-12-17T14:21:24Z2023-12-17T14:21:24Zhttps://npds.npdslinks.net/nexus/npds-root/solomonhttps://npds.npdslinks.net/nexus/npds-root/solomonhttps://npds.npdslinks.net/nexus/npds-root/solomonhttps://npds.npdslinks.net/nexus/npds-root/bha-scribe@{ Abstract=[In this review we present the most recent advances in nuclear medicine imaging as a diagnostic and management tool for dementia. The clinical diagnosis of dementia syndromes can be challenging for physicians, particularly in the early stages of disease. Given the growing number of individuals affected by dementia, early and accurate diagnosis can lead to improved clinical management of patients. Although tests are available for exclusion of certain causes of cognitive impairment, the results rarely allow the clinician to make a definitive diagnosis. For this reason, information obtained from imaging ("imaging biomarkers") is playing an increasingly important role in the workup of patients with suspected dementia. Imaging biomarkers also provide indispensable tools for clinical and preclinical studies of dementing illnesses to elucidate their pathophysiology and to develop better therapies. A wide range of imaging has been used to diagnose and investigate neurodegenerative disorders including structural, cerebral perfusion, glucose metabolism, neurochemical, and molecular imaging. In the first section, we discuss the imaging methods used in clinical practice to diagnose dementia as well as explore additional experimental modalities that are currently used as research tools. In the second section, a comprehensive review covering the myriad aspects of vascular disease as a cause of dementia is presented and illustrated with MRI- and PET-focused case examples. In the third section, advances in imaging Alzheimer disease pathology are emphasized by reviewing current approaches for PET imaging with ?-amyloid imaging agents. We provide an outline for the appropriate use criteria for ?-amyloid imaging agents in dementia. In addition, the recognition of the importance of neocortical neurofibrillary tangles as related to Alzheimer disease progression has led to the development of promising tau imaging agents such as [(18)F]T807. The last section provides a history brain trauma as a cause of chronic traumatic encephalopathy. Although the recognition of cognitive deficits from brain trauma dates back to the early part of last century, recent advances in our understanding of the neurobiology has led to the hope of developing molecular imaging methods for earlier diagnoses and treatment. This has become increasingly important given the raised public and physician awareness of the high incidence of this pathology in military conflicts and sports-related injuries. Overall advancements in nuclear medicine imaging have led to an improvement in the detection and accurate identification of dementia and its underlying causes. With both primary and secondary causes of dementia demonstrating often overlapping presentations, nuclear medicine imaging can play a key role not only in the diagnosis but the understanding of dementia. With earlier diagnosis and better understanding comes the hope of improved treatments or possibly someday a cure.], AbstractParsed=[In this review we present the most recent advances in nuclear medicine imaging as a diagnostic and management tool for dementia. The clinical diagnosis of dementia syndromes can be challenging for physicians, particularly in the early stages of disease. Given the growing number of individuals affected by dementia, early and accurate diagnosis can lead to improved clinical management of patients. Although tests are available for exclusion of certain causes of cognitive impairment, the results rarely allow the clinician to make a definitive diagnosis. For this reason, information obtained from imaging ("imaging biomarkers") is playing an increasingly important role in the workup of patients with suspected dementia. Imaging biomarkers also provide indispensable tools for clinical and preclinical studies of dementing illnesses to elucidate their pathophysiology and to develop better therapies. A wide range of imaging has been used to diagnose and investigate neurodegenerative disorders including structural, cerebral perfusion, glucose metabolism, neurochemical, and molecular imaging. In the first section, we discuss the imaging methods used in clinical practice to diagnose dementia as well as explore additional experimental modalities that are currently used as research tools. In the second section, a comprehensive review covering the myriad aspects of vascular disease as a cause of dementia is presented and illustrated with MRI- and PET-focused case examples. In the third section, advances in imaging Alzheimer disease pathology are emphasized by reviewing current approaches for PET imaging with ?-amyloid imaging agents. We provide an outline for the appropriate use criteria for ?-amyloid imaging agents in dementia. In addition, the recognition of the importance of neocortical neurofibrillary tangles as related to Alzheimer disease progression has led to the development of promising tau imaging agents such as [(18)F]T807. The last section provides a history brain trauma as a cause of chronic traumatic encephalopathy. Although the recognition of cognitive deficits from brain trauma dates back to the early part of last century, recent advances in our understanding of the neurobiology has led to the hope of developing molecular imaging methods for earlier diagnoses and treatment. This has become increasingly important given the raised public and physician awareness of the high incidence of this pathology in military conflicts and sports-related injuries. Overall advancements in nuclear medicine imaging have led to an improvement in the detection and accurate identification of dementia and its underlying causes. With both primary and secondary causes of dementia demonstrating often overlapping presentations, nuclear medicine imaging can play a key role not only in the diagnosis but the understanding of dementia. With earlier diagnosis and better understanding comes the hope of improved treatments or possibly someday a cure.], Author=[Eisenmenger, Laura B. and Huo, Eugene J. and Hoffman, John M. and Minoshima, Satoshi and Matesan, Manuela C. and Lewis, David H. and Lopresti, Brian J. and Mathis, Chester A. and Okonkwo, David O. and Mountz, James M.], CitationKey=[Eisenmenger2016], DOI=[10.1053/j.semnuclmed.2015.09.003], Institution=[University of Pittsburgh, Pittsburgh, PA. Electronic address: mountzjm@upmc.edu.], Journal=[Semin Nucl Med], KeywordsParsed=[], Language=[eng], ModificationDate=[2021-12-03T12:29:21], Month=[01], Number=[1], Pages=[57--87], PMID=[26687858], ReferenceType=[Article], Title=[Advances in PET Imaging of Degenerative, Cerebrovascular, and Traumatic Causes of Dementia.], TitleParsed=[Advances in PET Imaging of Degenerative, Cerebrovascular, and Traumatic Causes of Dementia.], URL=[http://dx.doi.org/10.1053/j.semnuclmed.2015.09.003], Volume=[46], Year=[2016], }@Public NPDS record with handle 'J8E349004' registered in 'SOLOMON ACMS' service by user with alias '' on 12/17/2023 6:21:24 AM.Distribution of 1-(2-deoxy-2-fluoro-beta-D-arabinofuranosyl) uracil in mice bearing colorectal cancer xenografts: rationale for therapeutic use and as a positron emission tomography probe for thymidylate synthase.In colorectal, breast, and head and neck cancers, response to 5-fluorouracil is associated with low expression of thymidylate synthase. In contrast, tumors with high expression of thymidylate synthase may be more sensitive to prodrugs such as 1-(2-deoxy-2-fluoro-beta-D-arabinofuranosyl) uracil (FAU) that are activated by thymidylate synthase. These studies were designed to evaluate FAU as a potential therapeutic and diagnostic probe.[18F]-FAU and [3H]-FAU were synthesized with >97\% radiochemical purity. [3H]-FAU or [18F]-FAU was administered intravenously to severe combined immunodeficient mice bearing either HT29 (low thymidylate synthase) or LS174T (high thymidylate synthase) human colon cancer xenografts. Four hours after [3H]-FAU dosing, tissue distribution of total radioactivity and incorporation of 1-(2-deoxy-2-fluoro-beta-D-arabinofuranosyl) 5-methyluracil (FMAU), derived from thymidylate synthase activation of FAU, into tumor DNA was measured. Positron emission tomography (PET) images were obtained fEiseman2004https://npds.brainwatch.net/nexus/solomon/eiseman2004Animals; Arabinofuranosyluracil, analogs /\&/ derivatives/diagnostic use/pharmacokinetics/therapeutic use; Colorectal Neoplasms, drug therapy/metabolism/pathology; DNA, Neoplasm, metabolism; Female; Fluorouracil, analogs /\&/ derivatives/diagnostic use/pha2023-12-17T14:20:53Z2023-12-17T14:20:54Zhttps://npds.npdslinks.net/nexus/npds-root/solomonhttps://npds.npdslinks.net/nexus/npds-root/solomonhttps://npds.npdslinks.net/nexus/npds-root/solomonhttps://npds.npdslinks.net/nexus/npds-root/bha-scribe@{ Abstract=[In colorectal, breast, and head and neck cancers, response to 5-fluorouracil is associated with low expression of thymidylate synthase. In contrast, tumors with high expression of thymidylate synthase may be more sensitive to prodrugs such as 1-(2-deoxy-2-fluoro-beta-D-arabinofuranosyl) uracil (FAU) that are activated by thymidylate synthase. These studies were designed to evaluate FAU as a potential therapeutic and diagnostic probe.[18F]-FAU and [3H]-FAU were synthesized with >97\% radiochemical purity. [3H]-FAU or [18F]-FAU was administered intravenously to severe combined immunodeficient mice bearing either HT29 (low thymidylate synthase) or LS174T (high thymidylate synthase) human colon cancer xenografts. Four hours after [3H]-FAU dosing, tissue distribution of total radioactivity and incorporation of 1-(2-deoxy-2-fluoro-beta-D-arabinofuranosyl) 5-methyluracil (FMAU), derived from thymidylate synthase activation of FAU, into tumor DNA was measured. Positron emission tomography (PET) images were obtained for 90 minutes after injection of [18F]-FAU. Thymidylate synthase activity was determined in vitro in tumors from untreated mice by [3H] release from [3H]dUMP. Each cell line was incubated in vitro with [3H]-FAU or [3H]-FMAU in the absence or presence of 5-fluoro-2'-deoxyuridine (FdUrd) and then was analyzed for incorporation of radiolabel into DNA.Thymidylate synthase enzymatic activity in LS174T xenografts was approximately 3.5-fold higher than in HT29 xenografts, and incorporation of radioactivity derived from [3H]-FAU into LS174T DNA was approximately 2-fold higher than into HT29 DNA. At 240 minutes, radioactivity derived from [3H]-FAU was approximately 2-fold higher in tumors than in skeletal muscle. At times up to 90 minutes, PET imaging detected only small differences in uptake of [18F]-FAU between the tumor types. Fluorine-18 in skeletal muscle was higher than in tumor for the first 90 minutes and plateaued earlier, whereas [18F] in tumor continued to increase during the 90-minute imaging period. For both cell lines in vitro, FdUrd decreased the rate of incorporation of [3H]-FAU into DNA, whereas the incorporation of [3H]-FMAU was increased.These results for FAU incorporation into DNA in vitro and in vivo further support clinical evaluation of FAU as a therapeutic agent in tumors with high concentrations of thymidylate synthase that are less likely to respond to 5-fluorouracil treatment. The high circulating concentrations of thymidine reported in mice may limit their utility in evaluating FAU as a PET probe.], AbstractParsed=[In colorectal, breast, and head and neck cancers, response to 5-fluorouracil is associated with low expression of thymidylate synthase. In contrast, tumors with high expression of thymidylate synthase may be more sensitive to prodrugs such as 1-(2-deoxy-2-fluoro-beta-D-arabinofuranosyl) uracil (FAU) that are activated by thymidylate synthase. These studies were designed to evaluate FAU as a potential therapeutic and diagnostic probe.[18F]-FAU and [3H]-FAU were synthesized with >97\% radiochemical purity. [3H]-FAU or [18F]-FAU was administered intravenously to severe combined immunodeficient mice bearing either HT29 (low thymidylate synthase) or LS174T (high thymidylate synthase) human colon cancer xenografts. Four hours after [3H]-FAU dosing, tissue distribution of total radioactivity and incorporation of 1-(2-deoxy-2-fluoro-beta-D-arabinofuranosyl) 5-methyluracil (FMAU), derived from thymidylate synthase activation of FAU, into tumor DNA was measured. Positron emission tomography (PET) images were obtained for 90 minutes after injection of [18F]-FAU. Thymidylate synthase activity was determined in vitro in tumors from untreated mice by [3H] release from [3H]dUMP. Each cell line was incubated in vitro with [3H]-FAU or [3H]-FMAU in the absence or presence of 5-fluoro-2'-deoxyuridine (FdUrd) and then was analyzed for incorporation of radiolabel into DNA.Thymidylate synthase enzymatic activity in LS174T xenografts was approximately 3.5-fold higher than in HT29 xenografts, and incorporation of radioactivity derived from [3H]-FAU into LS174T DNA was approximately 2-fold higher than into HT29 DNA. At 240 minutes, radioactivity derived from [3H]-FAU was approximately 2-fold higher in tumors than in skeletal muscle. At times up to 90 minutes, PET imaging detected only small differences in uptake of [18F]-FAU between the tumor types. Fluorine-18 in skeletal muscle was higher than in tumor for the first 90 minutes and plateaued earlier, whereas [18F] in tumor continued to increase during the 90-minute imaging period. For both cell lines in vitro, FdUrd decreased the rate of incorporation of [3H]-FAU into DNA, whereas the incorporation of [3H]-FMAU was increased.These results for FAU incorporation into DNA in vitro and in vivo further support clinical evaluation of FAU as a therapeutic agent in tumors with high concentrations of thymidylate synthase that are less likely to respond to 5-fluorouracil treatment. The high circulating concentrations of thymidine reported in mice may limit their utility in evaluating FAU as a PET probe.], Author=[Eiseman, Julie L. and Brown-Proctor, Clive and Kinahan, Paul E. and Collins, Jerry M. and Anderson, Lawrence W. and Joseph, Erin and Hamburger, Deborah R. and Pan, Su-Shu and Mathis, Chester A. and Egorin, Merrill J. and Klecker, Raymond W.], CitationKey=[Eiseman2004], DOI=[10.1158/1078-0432.CCR-03-0686], Institution=[Molecular Therapeutics/Drug Discovery Program, University of Pittsburgh Cancer Institute, Pittsburgh, Pennsylvania 15213-1863, USA. eisemanj@msx.upmc.edu], Journal=[Clin Cancer Res], Keywords=[Animals; Arabinofuranosyluracil, analogs /\&/ derivatives/diagnostic use/pharmacokinetics/therapeutic use; Colorectal Neoplasms, drug therapy/metabolism/pathology; DNA, Neoplasm, metabolism; Female; Fluorouracil, analogs /\&/ derivatives/diagnostic use/pharmacokinetics/therapeutic use; HT29 Cells; Humans; Mice; Mice, SCID; Positron-Emission Tomography; Thymidylate Synthase, metabolism; Time Factors; Tissue Distribution; Tritium; Xenograft Model Antitumor Assays, methods], KeywordsParsed=[Animals; Arabinofuranosyluracil, analogs /\&/ derivatives/diagnostic use/pharmacokinetics/therapeutic use; Colorectal Neoplasms, drug therapy/metabolism/pathology; DNA, Neoplasm, metabolism; Female; Fluorouracil, analogs /\&/ derivatives/diagnostic use/pharmacokinetics/therapeutic use; HT29 Cells; Humans; Mice; Mice, SCID; Positron-Emission Tomography; Thymidylate Synthase, metabolism; Time Factors; Tissue Distribution; Tritium; Xenograft Model Antitumor Assays, methods], Language=[eng], ModificationDate=[2021-12-03T12:29:21], Month=[10], Number=[19], Owner=[ctaswell], Pages=[6669--6676], PMID=[15475457], ReferenceType=[Article], TimeStamp=[2014.12.03], Title=[Distribution of 1-(2-deoxy-2-fluoro-beta-D-arabinofuranosyl) uracil in mice bearing colorectal cancer xenografts: rationale for therapeutic use and as a positron emission tomography probe for thymidylate synthase.], TitleParsed=[Distribution of 1-(2-deoxy-2-fluoro-beta-D-arabinofuranosyl) uracil in mice bearing colorectal cancer xenografts: rationale for therapeutic use and as a positron emission tomography probe for thymidylate synthase.], URL=[http://dx.doi.org/10.1158/1078-0432.CCR-03-0686], Volume=[10], Year=[2004], }@Public NPDS record with handle 'V75F7BAAF' registered in 'SOLOMON ACMS' service by user with alias '' on 12/17/2023 6:20:53 AM.Abnormal cerebral blood flow findings in transplant patients with posttransplant apraxia of speech.Eidelman2001https://npds.brainwatch.net/nexus/solomon/eidelman2001Apraxias, etiology/physiopathology; Basal Ganglia, blood supply/radionuclide imaging; Brain Ischemia, pathology; Brain, blood supply/pathology/radionuclide imaging; Cerebral Cortex, blood supply/pathology; Cerebrovascular Circulation; Cysteine, analogs /\&2023-12-17T14:20:23Z2023-12-17T14:20:23Zhttps://npds.npdslinks.net/nexus/npds-root/solomonhttps://npds.npdslinks.net/nexus/npds-root/solomonhttps://npds.npdslinks.net/nexus/npds-root/solomonhttps://npds.npdslinks.net/nexus/npds-root/bha-scribe@{ AbstractParsed=[], Author=[Eidelman, B. H. and Pulipaka, U. and Wiley, C. and Charron, M. and Bohnen, N. I.], CitationKey=[Eidelman2001], Institution=[University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania, USA.], Journal=[Transplant Proc], Keywords=[Apraxias, etiology/physiopathology; Basal Ganglia, blood supply/radionuclide imaging; Brain Ischemia, pathology; Brain, blood supply/pathology/radionuclide imaging; Cerebral Cortex, blood supply/pathology; Cerebrovascular Circulation; Cysteine, analogs /\&/ derivatives/diagnostic use; Female; Glial Fibrillary Acidic Protein, analysis; Heart Transplantation; Humans; Liver Transplantation; Magnetic Resonance Imaging; Male; Middle Aged; Organotechnetium Compounds, diagnostic use; Postoperative Complications; Radiopharmaceuticals, diagnostic use; Speech; Thalamus, blood supply/radionuclide imaging; Tomography, Emission-Computed, Single-Photon], KeywordsParsed=[Apraxias, etiology/physiopathology; Basal Ganglia, blood supply/radionuclide imaging; Brain Ischemia, pathology; Brain, blood supply/pathology/radionuclide imaging; Cerebral Cortex, blood supply/pathology; Cerebrovascular Circulation; Cysteine, analogs /\&/ derivatives/diagnostic use; Female; Glial Fibrillary Acidic Protein, analysis; Heart Transplantation; Humans; Liver Transplantation; Magnetic Resonance Imaging; Male; Middle Aged; Organotechnetium Compounds, diagnostic use; Postoperative Complications; Radiopharmaceuticals, diagnostic use; Speech; Thalamus, blood supply/radionuclide imaging; Tomography, Emission-Computed, Single-Photon], Language=[eng], ModificationDate=[2021-12-03T12:29:21], Month=[6], Number=[4], Owner=[ctaswell], Pages=[2563--2565], PMID=[11406249], ReferenceType=[Article], TimeStamp=[2014.11.26], Title=[Abnormal cerebral blood flow findings in transplant patients with posttransplant apraxia of speech.], TitleParsed=[Abnormal cerebral blood flow findings in transplant patients with posttransplant apraxia of speech.], Volume=[33], Year=[2001], }@Public NPDS record with handle 'N10D100D3' registered in 'SOLOMON ACMS' service by user with alias '' on 12/17/2023 6:20:23 AM.