﻿<?xml version="1.0" encoding="utf-8"?><NPDS Version="2.4.2 (2025-09-13)" xmlns="http://npds.portaldoors.org/schema/pdp/npds#"><!--Nexus-PORTAL-DOORS-Scribe Cyberinfrastructure System (c) 2006-2026 Carl Taswell and the PORTAL-DOORS Project Team--><ClientRequest><URL>https://www.npdslinks.net/Nexus/SOLOMON?ef=1&amp;lc=11&amp;vf=1</URL><Note /><Question /></ClientRequest><ServerResponse><Status /><Note /><Answer /><Related /><Referred /></ServerResponse><AtlasServer Count="0" /><PortalServer Count="0" /><DoorsServer Count="0" /><NexusServer><NexusService Count="11"><NexusResRep IsAuthorPrivate="false" IsAgentShared="false" IsUpdaterLimited="false" IsManagerReleased="false"><EntityMetadata><Name>Dissociable neural responses in human reward systems.</Name><Nature>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 incr</Nature><PrincipalTag>Elliott2000</PrincipalTag><CanonicalLabel EntityType="Publication">https://npds.brainwatch.net/nexus/solomon/elliott2000</CanonicalLabel><AliasLabels Count="0" /></EntityMetadata><RecordMetadata><CreatedOn>2023-12-17T14:25:27Z</CreatedOn><UpdatedOn>2023-12-17T14:25:28Z</UpdatedOn><Diristry>https://npds.npdslinks.net/nexus/npds-root/solomon</Diristry><Registrar>https://npds.npdslinks.net/nexus/npds-root/bha-scribe</Registrar><Registrant /><Signatures Count="0" /></RecordMetadata><InfosetMetadata /></NexusResRep><NexusResRep IsAuthorPrivate="false" IsAgentShared="false" IsUpdaterLimited="false" IsManagerReleased="false"><EntityMetadata><Name>Management impact of FDG-PET in dementia: results from a tertiary center memory clinic.</Name><Nature /><PrincipalTag>Elias2014</PrincipalTag><CanonicalLabel EntityType="Publication">https://npds.brainwatch.net/nexus/solomon/elias2014</CanonicalLabel><AliasLabels Count="0" /></EntityMetadata><RecordMetadata><CreatedOn>2023-12-17T14:24:57Z</CreatedOn><UpdatedOn>2023-12-17T14:24:57Z</UpdatedOn><Diristry>https://npds.npdslinks.net/nexus/npds-root/solomon</Diristry><Registrar>https://npds.npdslinks.net/nexus/npds-root/bha-scribe</Registrar><Registrant /><Signatures Count="0" /></RecordMetadata><InfosetMetadata /></NexusResRep><NexusResRep IsAuthorPrivate="false" IsAgentShared="false" IsUpdaterLimited="false" IsManagerReleased="false"><EntityMetadata><Name>Quantitative SPECT leads to improved performance in discrimination tasks related to prodromal Alzheimer's disease.</Name><Nature>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 follow</Nature><PrincipalTag>ElFakhri2004</PrincipalTag><CanonicalLabel EntityType="Publication">https://npds.brainwatch.net/nexus/solomon/elfakhri2004</CanonicalLabel><AliasLabels Count="0" /></EntityMetadata><RecordMetadata><CreatedOn>2023-12-17T14:24:26Z</CreatedOn><UpdatedOn>2023-12-17T14:24:27Z</UpdatedOn><Diristry>https://npds.npdslinks.net/nexus/npds-root/solomon</Diristry><Registrar>https://npds.npdslinks.net/nexus/npds-root/bha-scribe</Registrar><Registrant /><Signatures Count="0" /></RecordMetadata><InfosetMetadata /></NexusResRep><NexusResRep IsAuthorPrivate="false" IsAgentShared="false" IsUpdaterLimited="false" IsManagerReleased="false"><EntityMetadata><Name>MRI-guided SPECT perfusion measures and volumetric MRI in prodromal Alzheimer disease.</Name><Nature>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 discrimi</Nature><PrincipalTag>ElFakhri2003</PrincipalTag><CanonicalLabel EntityType="Publication">https://npds.brainwatch.net/nexus/solomon/elfakhri2003</CanonicalLabel><AliasLabels Count="0" /></EntityMetadata><RecordMetadata><CreatedOn>2023-12-17T14:23:56Z</CreatedOn><UpdatedOn>2023-12-17T14:23:56Z</UpdatedOn><Diristry>https://npds.npdslinks.net/nexus/npds-root/solomon</Diristry><Registrar>https://npds.npdslinks.net/nexus/npds-root/bha-scribe</Registrar><Registrant /><Signatures Count="0" /></RecordMetadata><InfosetMetadata /></NexusResRep><NexusResRep IsAuthorPrivate="false" IsAgentShared="false" IsUpdaterLimited="false" IsManagerReleased="false"><EntityMetadata><Name>Spatial and temporal variability in VOC levels within a commercial retail building.</Name><Nature>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 compou</Nature><PrincipalTag>Eklund2008</PrincipalTag><CanonicalLabel EntityType="Publication">https://npds.brainwatch.net/nexus/solomon/eklund2008</CanonicalLabel><AliasLabels Count="0" /></EntityMetadata><RecordMetadata><CreatedOn>2023-12-17T14:23:25Z</CreatedOn><UpdatedOn>2023-12-17T14:23:26Z</UpdatedOn><Diristry>https://npds.npdslinks.net/nexus/npds-root/solomon</Diristry><Registrar>https://npds.npdslinks.net/nexus/npds-root/bha-scribe</Registrar><Registrant /><Signatures Count="0" /></RecordMetadata><InfosetMetadata /></NexusResRep><NexusResRep IsAuthorPrivate="false" IsAgentShared="false" IsUpdaterLimited="false" IsManagerReleased="false"><EntityMetadata><Name>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.</Name><Nature>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 scan</Nature><PrincipalTag>Eisenstein2017</PrincipalTag><CanonicalLabel EntityType="Publication">https://npds.brainwatch.net/nexus/solomon/eisenstein2017</CanonicalLabel><AliasLabels Count="0" /></EntityMetadata><RecordMetadata><CreatedOn>2023-12-17T14:22:55Z</CreatedOn><UpdatedOn>2023-12-17T14:22:55Z</UpdatedOn><Diristry>https://npds.npdslinks.net/nexus/npds-root/solomon</Diristry><Registrar>https://npds.npdslinks.net/nexus/npds-root/bha-scribe</Registrar><Registrant /><Signatures Count="0" /></RecordMetadata><InfosetMetadata /></NexusResRep><NexusResRep IsAuthorPrivate="false" IsAgentShared="false" IsUpdaterLimited="false" IsManagerReleased="false"><EntityMetadata><Name>Correction: Insulin, Central Dopamine D2 Receptors, and Monetary Reward Discounting in Obesity.</Name><Nature /><PrincipalTag>Eisenstein2016a</PrincipalTag><CanonicalLabel EntityType="Publication">https://npds.brainwatch.net/nexus/solomon/eisenstein2016a</CanonicalLabel><AliasLabels Count="0" /></EntityMetadata><RecordMetadata><CreatedOn>2023-12-17T14:22:24Z</CreatedOn><UpdatedOn>2023-12-17T14:22:25Z</UpdatedOn><Diristry>https://npds.npdslinks.net/nexus/npds-root/solomon</Diristry><Registrar>https://npds.npdslinks.net/nexus/npds-root/bha-scribe</Registrar><Registrant /><Signatures Count="0" /></RecordMetadata><InfosetMetadata /></NexusResRep><NexusResRep IsAuthorPrivate="false" IsAgentShared="false" IsUpdaterLimited="false" IsManagerReleased="false"><EntityMetadata><Name>Prediction of striatal D2 receptor binding by DRD2/ANKK1 TaqIA allele status.</Name><Nature>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 s</Nature><PrincipalTag>Eisenstein2016</PrincipalTag><CanonicalLabel EntityType="Publication">https://npds.brainwatch.net/nexus/solomon/eisenstein2016</CanonicalLabel><AliasLabels Count="0" /></EntityMetadata><RecordMetadata><CreatedOn>2023-12-17T14:21:54Z</CreatedOn><UpdatedOn>2023-12-17T14:21:54Z</UpdatedOn><Diristry>https://npds.npdslinks.net/nexus/npds-root/solomon</Diristry><Registrar>https://npds.npdslinks.net/nexus/npds-root/bha-scribe</Registrar><Registrant /><Signatures Count="0" /></RecordMetadata><InfosetMetadata /></NexusResRep><NexusResRep IsAuthorPrivate="false" IsAgentShared="false" IsUpdaterLimited="false" IsManagerReleased="false"><EntityMetadata><Name>Advances in PET Imaging of Degenerative, Cerebrovascular, and Traumatic Causes of Dementia.</Name><Nature>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, cereb</Nature><PrincipalTag>Eisenmenger2016</PrincipalTag><CanonicalLabel EntityType="Publication">https://npds.brainwatch.net/nexus/solomon/eisenmenger2016</CanonicalLabel><AliasLabels Count="0" /></EntityMetadata><RecordMetadata><CreatedOn>2023-12-17T14:21:24Z</CreatedOn><UpdatedOn>2023-12-17T14:21:24Z</UpdatedOn><Diristry>https://npds.npdslinks.net/nexus/npds-root/solomon</Diristry><Registrar>https://npds.npdslinks.net/nexus/npds-root/bha-scribe</Registrar><Registrant /><Signatures Count="0" /></RecordMetadata><InfosetMetadata /></NexusResRep><NexusResRep IsAuthorPrivate="false" IsAgentShared="false" IsUpdaterLimited="false" IsManagerReleased="false"><EntityMetadata><Name>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.</Name><Nature>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 &gt;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 f</Nature><PrincipalTag>Eiseman2004</PrincipalTag><CanonicalLabel EntityType="Publication">https://npds.brainwatch.net/nexus/solomon/eiseman2004</CanonicalLabel><AliasLabels Count="0" /></EntityMetadata><RecordMetadata><CreatedOn>2023-12-17T14:20:53Z</CreatedOn><UpdatedOn>2023-12-17T14:20:54Z</UpdatedOn><Diristry>https://npds.npdslinks.net/nexus/npds-root/solomon</Diristry><Registrar>https://npds.npdslinks.net/nexus/npds-root/bha-scribe</Registrar><Registrant /><Signatures Count="0" /></RecordMetadata><InfosetMetadata /></NexusResRep><NexusResRep IsAuthorPrivate="false" IsAgentShared="false" IsUpdaterLimited="false" IsManagerReleased="false"><EntityMetadata><Name>Abnormal cerebral blood flow findings in transplant patients with posttransplant apraxia of speech.</Name><Nature /><PrincipalTag>Eidelman2001</PrincipalTag><CanonicalLabel EntityType="Publication">https://npds.brainwatch.net/nexus/solomon/eidelman2001</CanonicalLabel><AliasLabels Count="0" /></EntityMetadata><RecordMetadata><CreatedOn>2023-12-17T14:20:23Z</CreatedOn><UpdatedOn>2023-12-17T14:20:23Z</UpdatedOn><Diristry>https://npds.npdslinks.net/nexus/npds-root/solomon</Diristry><Registrar>https://npds.npdslinks.net/nexus/npds-root/bha-scribe</Registrar><Registrant /><Signatures Count="0" /></RecordMetadata><InfosetMetadata /></NexusResRep></NexusService></NexusServer></NPDS>