ABSTRACT
Impedance cardiography is a technique commonly used in psychophysiological studies. However, concerns about the utility of full circumferential band electrodes (FB) have been raised. The current study was designed to compare FB with a three-quarter circumferential band configuration (PB). A total of 47 participants (66% female, mean [SD] age=20.4 [3.0] years) underwent 2 testing sessions, once using FB and once using PB. Session order was randomized and balanced. Each session consisted of 5 min of rest, math task, recovery, and cold pressor test. Average baseline and task pre-ejection period (PEP), stroke volume (SV), cardiac output (CO), heart rate (HR), blood pressure (BP), and total peripheral resistance (TPR) was calculated from impedance cardiography and blood pressure monitoring. Participants were are asked to rate measures of comfort after each session. There were no significant difference between the mean levels of PEP, SV, CO, HR, and TPR for the PB versus the FB configurations. However, both systolic BP and diastolic BP were higher during the FB session. Intraclass correlations were high (r(icc) =.63-.93) between PB and FB. Bland-Altman analyses revealed a low level of bias (≤5%) between the configurations. Based on limits of agreement between ±30%, there was equivalence in PEP between the 2 configurations, and SV, CO, and TPR were close to reaching equivalence. Participants clearly indicated greater comfort with the PB configuration compared to the FB. The current study provides incremental evidence that suggests a three-quarter PB configuration may be utilized for standard psychophysiological testing instead of the standard FB configuration. However, further studies are needed to validate the PB configuration against other techniques.
Subject(s)
Cardiography, Impedance/methods , Analysis of Variance , Cardiography, Impedance/statistics & numerical data , Cold Temperature , Data Interpretation, Statistical , Electrodes , Female , Hemodynamics/physiology , Humans , Male , Pain Measurement , Pressure , Signal Processing, Computer-Assisted , Stress, Psychological/physiopathology , Young AdultABSTRACT
Perinatal hypoxic-ischemic encephalopathy results in a spectrum of pathologies related to the degree of initial infarct and environmental factors, including maternal interactions. Infants actively influence their environment by crying; rat pups produce ultrasonic vocalizations (USVs). Our study observed that ischemic pups engage in less time producing USVs and make fewer USVs overall, with male ischemic pups experiencing reductions in more categories than females. Future studies should consider whether alterations in mother-pup interactions result from these reductions.
Subject(s)
Hypoxia-Ischemia, Brain/physiopathology , Social Isolation , Vocalization, Animal/physiology , Animals , Animals, Newborn , Disease Models, Animal , Female , Male , Random Allocation , Rats , Rats, Wistar , Sex Factors , Social Environment , UltrasonicsABSTRACT
The proteinase-activated receptors (PARs) are a novel family of G protein-coupled receptors, and their effects in neurodegenerative diseases remain uncertain. Alzheimer's disease (AD) is a neurodegenerative disorder defined by misfolded protein accumulation with concurrent neuroinflammation and neuronal death. We report suppression of proteinase-activated receptor-2 (PAR2) expression in neurons of brains from AD patients, whereas PAR2 expression was increased in proximate glial cells, together with up-regulation of proinflammatory cytokines and chemokines and reduced IL-4 expression (p < 0.05). Glial PAR2 activation increased expression of formyl peptide receptor-2 (p < 0.01), a cognate receptor for a fibrillar 42-aa form of beta-amyloid (Abeta(1-42)), enhanced microglia-mediated proinflammatory responses, and suppressed astrocytic IL-4 expression, resulting in neuronal death (p < 0.05). Conversely, neuronal PAR2 activation protected human neurons against the toxic effects of Abeta(1-42) (p < 0.05), a key component of AD neuropathogenesis. Amyloid precursor protein-transgenic mice, displayed glial fibrillary acidic protein and IL-4 induction (p < 0.05) in the absence of proinflammatory gene up-regulation and neuronal injury, whereas PAR2 was up-regulated at this early stage of disease progression. PAR2-deficient mice, after hippocampal Abeta(1-42) implantation, exhibited enhanced IL-4 induction and less neuroinflammation (p < 0.05), together with improved neurobehavioral outcomes (p < 0.05). Thus, PAR2 exerted protective properties in neurons, but its activation in glia was pathogenic with secretion of neurotoxic factors and suppression of astrocytic anti-inflammatory mechanisms contributing to Abeta(1-42)-mediated neurodegeneration.