Pentosidine is a fluorescent advanced Maillard/glycosylation product and protein cross-link present in elevated amounts in skin from diabetic and uremic subjects. A high-performance liquid chromatographic (HPLC) assay was developed to quantitate pentosidine in plasma and erythrocytes and other tissue proteins with low levels of pentosidine. High protein content and presence of basic amino acids and O2 during acid hydrolysis led to the formation of fluorescent artifacts that could be separated from true pentosidine through combined reverse-phase ion-exchange HPLC. No true pentosidine was formed during acid hydrolysis of ribated protein, suggesting that Amadori products do not generate artifactual pentosidine during hydrolysis. With the combined reverse-phase ion-exchange chromatographic assay, we found a 2.5-fold (P less than 0.001) and a 23-fold (P less than 0.001) elevation of mean +/- SD plasma protein pentosidine in diabetic (2.4 +/- 1.2 pmol/mg) and uremic (21.5 +/- 10.8 pmol/mg) subjects compared with healthy (0.95 +/- 0.33 pmol/mg) subjects. Pentosidine in hemolysate was normal in diabetes but dramatically elevated in uremia (0.6 +/- 0.4 pmol/mg hemoglobin, P less than 0.001). Although the precise nature of the pentosidine precursor sugar is unknown, plasma pentosidine may be a useful marker for monitoring the biochemical efficacy of trials with aminoguanidine or other treatment modalities. Furthermore, pentosidine in plasma proteins may act as a signal for advanced glycosylation end product-mediated receptor uptake by macrophages and other cells and contribute to accelerated atherosclerosis in diabetes and uremia.

Background: In resting-state EEG, the ratio between frontal power in the slow theta frequency band and the fast beta frequency band (the theta/beta ratio, TBR) has previously been negatively related to attentional control. Also, increased theta and reduced beta power were observed during mind wandering (MW) compared to episodes of focused attention. Thus, increased resting-state frontal TBR could be related to MW, suggesting that previously observed relationships between TBR and attentional control could reflect MW episodes increasing the average resting state TBR in people with low attentional control. Goals: To replicate and extend the previous theta and beta MW effects for frontal TBR recordings and test if MW related changes in frontal TBR are related to attentional control. Methods: Twenty-six healthy participants performed a 40-minute breath-counting task, after a baseline EEG recording, while EEG was measured and participants indicated MW episodes with button presses. Results: Frontal TBR was significantly higher during MW episodes than during on-task periods. However, no relation between frontal TBR and attentional control was found. Conclusions: This confirms that frontal TBR varies with MW episodes and that previous frontal TBRattentional control relations might be related to MW, though no direct evidence was found for this hypothesis.

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This study investigated stimulus‐response patterns of temporal principal components analysis (PCA)–derived event‐related potential (ERP) components in a classical auditory habituation paradigm with long interstimulus intervals. The skin conductance response (SCR) was included as the “gold standard” model of the Orienting Reflex. Thirty participants were presented with a single series of 10 identical 60 dB tones, followed by a change trial at a different frequency. Single‐trial, electrooculography‐corrected ERPs were submitted to temporal PCA. The main focus was on the components expected in the P300/Late Positive Complex (LPC), and their electromagnetic tomography–derived cortical sources. Nine components were identified between 90 and 470 ms poststimulus (in temporal order): three N1 subcomponents, P2, four LPC components, and a negative Slow Wave (SW). The expected order of P3a, P3b, Novelty P3 (nP3), and positive Slow Wave (+SW) in the LPC was confirmed. SCR demonstrated strong exponential decay and recovery. P3b and nP3 each showed exponential decrement over trials, but only nP3 showed recovery at the change trial. Novelty effects failed to reach significance for the other LPC components, and were not apparent in non‐LPC components. Frontal lobe activity in Brodmann areas 6, 8, and 9 was common to P3a, P3b, nP3, and +SW, consistent with the functional integration of these components in the LPC. Individual components had specific sources, although some sources overlapped between components or were reactivated later in the LPC. These data provide a fresh perspective on the components of the LPC and their cortical sources, and offer a processing model for the P300 in a habituation task, potentially generalizable to other paradigms.

Heightened pain sensitivity, the amount of pain experienced in response to a noxious event, is a known risk factor for development of chronic pain. We have previously reported that pain-free, sensorimotor peak alpha frequency (PAF) is a reliable biomarker of pain sensitivity for thermal, prolonged pains lasting tens of minutes. To test whether PAF can provide information about pain sensitivity occurring over clinically relevant timescales (i.e., weeks), EEG was recorded before and while participants experienced a long-lasting pain model, repeated intramuscular injection of nerve growth factor (NGF), that produces progressively developing muscle pain for up to 21 days. We demonstrate that pain-free, sensorimotor PAF is negatively correlated with NGF pain sensitivity; increasingly slower PAF is associated with increasingly greater pain sensitivity. Furthermore, PAF remained stable following NGF injection, indicating that the presence of NGF pain for multiple weeks is not sufficient to induce the PAF slowing reported in chronic pain. In total, our results demonstrate that slower pain-free, sensorimotor PAF is associated with heightened sensitivity to a long-lasting musculoskeletal pain and also suggest that the apparent slowing of PAF in chronic pain may reflect predisease pain sensitivity. NEW & NOTEWORTHY Pain sensitivity, the intensity of pain experienced after injury, has been identified as an important risk factor in the development of chronic pain. Biomarkers of pain sensitivity have the potential to ease chronic pain burdens by preventing disease emergence. In the current study, we demonstrate that the speed of pain-free, sensorimotor peak alpha frequency recorded during resting-state EEG predicts pain sensitivity to a clinically-relevant, human model of prolonged pain that persists for weeks.