Association Between Risk of Obstructive Sleep Apnea and Cerebrovascular Reactivity in Stroke Patients.

Background Obstructive sleep apnea (OSA) is present in 60% to 70% of stroke patients. Cerebral vasoreactivity in patients with stroke and OSA has not been well studied and could identify a new pathophysiologic mechanism with potential therapeutic intervention. We aimed to determine whether risk categories for OSA are associated with cerebral vasoreactivity in stroke patients. Methods and Results In this cross-sectional study of a cohort of patients with stroke, we used clinical questionnaires (Sleep Obstructive Apnea Score Optimized for Stroke [SOS] and snoring, tiredness, observed, pressure, bmi, age, neck, gender [STOP-BANG] scores) to assess the risk of OSA and transcranial Doppler to assess cerebral vasoreactivity (breath-holding index and visual evoked flow velocity response). Of the 99 patients included, 77 (78%) had medium or high risk of OSA and 80 performed transcranial Doppler. Mean breath-holding index was 0.52±0.37, and median visual evoked flow velocity response was 10.8% (interquartile range: 8.8-14.5); 54 of 78 (69%) showed impaired anterior circulation vasoreactivity (breath-holding index <0.69) and 53 of 71 (75%) showed impaired posterior circulation vasoreactivity (visual evoked flow velocity response ≤14.0%). There was a significant negative correlation between the risk of OSA calculated by STOP-BANG and the breath-holding index (rS=-0.284, P=0.012). The following variables were associated with low anterior circulation vasoreactivity: dyslipidemia (odds ratio: 4.7; 95% CI, 1.5-14.2) and STOP-BANG score (odds ratio: 1.7 per 1-point increase; 95% CI, 1.1-1.5). Conclusions A high risk of OSA and impaired vasoreactivity exists in the population that has had stroke. Dyslipidemia and STOP-BANG sleep apnea risk categories were independently associated with impaired anterior circulation vasoreactivity.

Inhibitory Selection Mechanisms in Clinically Healthy Older and Younger Adults.

Objective: Declines in working memory are a ubiquitous finding within the cognitive-aging literature. A unitary inhibitory selection mechanism that serves to guide attention toward task-relevant information and resolve interference from task-irrelevant information has been proposed to underlie such deficits. However, inhibition can occur at multiple time points in the memory-processing stream. Here, we tested whether the time point at which inhibition occurs in the memory-processing stream affects age-related memory decline. Method: Clinically healthy younger (n = 23) and older (n = 22) adults performed two similar item-recognition working memory tasks. In one task, participants received an instruction cue telling them which words to attend to followed by a memory set, promoting perceptual inhibition at the time of encoding. In the other task, participants received the instruction cue after they received the memory set, fostering inhibition of items already in memory. Results: We found that older and younger adults differed in their ability to inhibit items both during encoding and when items had to be inhibited in memory but that these age differences were exaggerated when irrelevant information had to be inhibited from memory. These results provide insights into the mechanisms that support cognitive changes to memory processes in healthy aging.

A CFA-Induced Model of Inflammatory Skin Disease in Miniature Swine.

Similarities between porcine and human skin make the pig an ideal model for preclinical studies of cutaneous inflammation and wound healing. Complete Freund's adjuvant (CFA) has been used to induce inflammation and to study inflammatory pain in several animal models. Here, we evaluated the inflammation caused by CFA injected in different layers of skin and subcutaneous (SC) tissue in a large-animal model. The degree of inflammation was evaluated at early and late time points by visual inspection and histopathologic analysis. In addition, the side effects of CFA injections were evaluated based on clinical findings, behavioral changes, physiologic state, and (histo)pathologic lesions. Pigs were injected with CFA at the back of the neck's skin at different depths. All animals showed histologic signs of inflammation at the injection site. Animals injected SC did not show any signs of pain or distress (loss of appetite, abnormal behavior) and did not require pain medication. Inflammation was followed by measuring the area of induration beneath the skin. Animals injected into the dermis and/or epidermis demonstrated a severe inflammatory response on the skin surface with massive swelling, redness within 12hrs of CFA injection, and severe skin necrosis within a week, preventing accurate induration measurements. In contrast to animals injected SC, animals receiving intradermal and/or intraepidermal injection of CFA showed signs of distress requiring pain medication. Conclusion. SC injection of CFA in swine induces an inflammatory response that can be measured accurately by induration without causing unnecessary discomfort, providing a useful preclinical large-animal model of inflammatory skin disease.

Non-invasive monitoring of skin inflammation using an oxygen-sensing paint-on bandage.

Inflammation involves a cascade of cellular and molecular mediators that ultimately lead to the infiltration of immune cells into the affected area. This inflammatory process in skin is common to many diseases including acne, infection, and psoriasis, with the presence or absence of immune cells a potential diagnostic marker. Here we show that skin inflammation can be non-invasively measured and mapped using a paint-on oxygen sensing bandage in an in vivo porcine inflammation model. After injection of a known inflammatory agent, the bandage could track the increase, plateau, and decrease in oxygen consumption at the injury site over 7 weeks, as well as discern inflammation resultant from injection at various depths beneath the surface of the skin. Both the initial rate of pO2 change and the change in bandage pO2 at equilibration (CBP20) were found to be directly related to the metabolic oxygen consumption rate of the tissue in contact. Healthy skin demonstrated an initial pO2 decrease rate of 6.5 [Formula: see text], and CBP20 of 84 [Formula: see text]. Inflamed skin had a significantly higher initial consumption rate of 55 [Formula: see text], and a larger CBP20 of 140 [Formula: see text]. The change in the bandage pO2 before and after equilibration with tissue was found to correlate well with histological evidence of skin inflammation in the animals.