82 research outputs found

    Face Processing in the Chimpanzee Brain

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    SummaryHuman face recognition involves highly specialized cognitive and neural processes that enable the recognition of specific individuals [1–5]. Although comparative studies suggest that similar cognitive processes underlie face recognition in chimpanzees and humans ([6–8] and Supplemental Data), it remains unknown whether chimpanzees also show face-selective activity in ventral temporal cortex. This study is the first to examine regional cerebral glucose metabolism with 18F-flurodeoxyglucose positron emission tomography in chimpanzees after they performed computerized tasks matching conspecifics' faces and nonface objects (Supplemental Data). A whole-brain analysis comparing these two tasks in five chimpanzees revealed significant face-selective activity in regions known to comprise the distributed cortical face-processing network in humans, including superior temporal sulcus and orbitofrontal cortex [9–11]. In order to identify regions that were exclusively active during one task, but not the other, we subtracted a resting-state condition from each task and identified the activity exclusive to each. This revealed numerous distinct patches of face-selective activity in the fusiform gyrus that were interspersed within a large expanse of object-selective cortex. This pattern suggests similar object form topography in the ventral temporal cortex of chimpanzees and humans, in which faces may represent a special class of visual stimulus

    Role of Dopamine Transporters in the Behavioral Effects of 3,4-Methylenedioxymethamphetamine (MDMA) in Nonhuman Primates

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    RATIONALE: The interoceptive and reinforcing effects of 3,4-methylenedioxymethamphetamine (MDMA) are similar to those of psychostimulants, but the role of dopamine in the behavioral effects of MDMA is not well documented, especially in primates. OBJECTIVE: The aim of this study was to assess the role of dopamine in the behavioral effects of MDMA in two nonhuman primate species. METHODS: The behavioral effects of MDMA, with and without serotonergic or dopaminergic pretreatments, were studied in squirrel monkeys trained to respond under a fixed-interval schedule of stimulus termination; effects on caudate dopamine levels were studied in a separate group of squirrel monkeys using in vivo microdialysis. Positron emission tomography neuroimaging with the dopamine transporter (DAT) ligand [18F]FECNT was used to determine DAT occupancy by MDMA in rhesus monkeys. RESULTS: MDMA (0.5-1.5 mg/kg) did not induce behavioral stimulant effects, but the highest dose of MDMA suppressed responding. Pretreatment with fluoxetine (3.0 mg/kg) or the selective 5HT(2A) antagonist M100907 (0.03-0.3 mg/kg) attenuated the rate suppressing effects of MDMA. In contrast, pretreatment with the selective dopamine transporter inhibitor RTI-177 (0.1 mg/kg) did not alter the rate suppressing effects of MDMA. Administration of MDMA at a dose that suppressed operant behavior had negligible effects on extracellular dopamine. The percent DAT occupancy of MDMA at a dose that suppressed operant behavior also was marginal and reflected low in vivo potency for DAT binding. CONCLUSIONS: Collectively, these results indicate that behaviorally relevant doses of MDMA do not induce behavioral stimulant or dopamine transporter-mediated effects in nonhuman primates

    Endothelial dysfunction is associated with occult coronary artery disease detected by positron emission tomography

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    Objective: Silent myocardial ischemia is common in asymptomatic subjects without a prior history of coronary artery disease (CAD) and is associated with increased morbidity and mortality. Our objective was to determine whether endothelial dysfunction is associated with silent myocardial ischemia and whether the association is independent of genetic and familial factors. Material and methods: We examined 416 male monozygotic and dizygotic twins aged 47 to 63 years, free of symptomatic CAD. Subclinical ischemia was diagnosed by [13N] ammonia positron emission tomography at rest and after adenosine stress. Endothelial function was measured by flow-mediated dilation (FMD) of the brachial artery. Generalized estimating equations were used for analysis. Results: Fixed perfusion defects were found in 24 (6%) twins and reversible perfusion defects in 90 (22%) twins, indicating subclinical ischemia. There was an inverse correlation between FMD and the reversible perfusion defect score (r = − 0.14, p = 0.01) but not the fixed defect score (r = − 0.017, p = 0.73). From the lowest to the highest quartiles of FMD, the prevalence of reversible defects decreased from 28% to 14%, p = 0.008. In multivariable analysis, reversible defects were significantly associated with each quartile of decreasing FMD (OR = 1.3; 95% 1.1, 2.5). In 54 twin pairs discordant for endothelial dysfunction (FMD ≤ 7% dilation from baseline), twins with endothelial dysfunction had 9% higher likelihood of having perfusion defects than their co-twins without endothelial dysfunction (p = 0.041). Conclusions: Endothelial dysfunction is independently associated with silent ischemia and this association is not confounded by genetic or other shared familial factors

    Posttraumatic Stress Disorder and Incidence of Coronary Heart Disease: A Twin Study

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    OBJECTIVES: To determine whether posttraumatic stress disorder (PTSD) is associated with coronary heart disease (CHD) using a prospective twin study design and objective measures of CHD. BACKGROUND: It has long been hypothesized that PTSD increases the risk of CHD but empirical evidence using objective measures is limited. METHODS: We conducted a prospective study of middle-aged male twins from the Vietnam Era Twin Registry. Among twin pairs without self-reported CHD at baseline, we selected pairs discordant for a lifetime history of PTSD, pairs discordant for a lifetime history of major depression, and pairs without either condition. All underwent a clinic visit after a median follow-up of 13 years. Outcomes included clinical events (myocardial infarction, other hospitalizations for CHD and coronary revascularization) and quantitative measures of myocardial perfusion by [N13] positron emission tomography, including a stress total severity score (STSS) and coronary flow reserve (CFR). RESULTS: A total of 562 twins (281 pairs) were included with mean age of 42.6 yrs at baseline. The incidence of CHD was more than double in twins with PTSD (22.6%) than those without PTSD (8.9%; p<0.001). The association remained robust after adjusting for lifestyle factors, other CHD risk factors and major depression (OR=2.2, 95% confidence interval, 1.2-4.1). STSS was significantly higher (+ 95%, p=0.001) and CFR lower (−0.21, p=0.02) in twins with PTSD than those without, denoting worse myocardial perfusion. Associations were only mildly attenuated within 117 twin pairs discordant for PTSD. CONCLUSIONS: Among Vietnam era veterans, PTSD is a risk factor for CHD

    Pleural Effusion in Multiple Myeloma

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    Two patients with multiple myeloma are described in whom an unusual complication developed: pleural effusion containing myeloma cells. There are 7 previously reported cases of myeloma in the English literature with this type of effusion. Pleural effusion in myeloma may be due to plasma cell infiltration of the pleura, congestive heart failure, pulmonary embolism, nephrotic syndrome, and second neoplasms. In view of these multiple etiologies, diagnostic thoracentesis should be performed in order to treat the effusion appropriately

    Technical aspects of acquiring and measuring myocardial blood flow: Method, technique, and QA

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    Measuring absolute myocardial blood flow (MBF) is becoming a common aid for diagnosing patients suspected to have coronary artery disease. An MBF study, however, requires a scanner with high count rate capability, is more susceptible to artifacts, and is much more technically involved than static imaging, which leads to a greater risk of artifactual results contaminating the final result. This technical note gives the reader an introductory understanding of the method for calculating MBF. It then describes the scanning protocol, potential pitfalls and how to recognize them, and quality control steps that should be taken to avoid basing a clinical decision on possibly inaccurate flow information
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