The endothelial glycocalyx is a dynamic structure integral to blood vessel hemodynamics and capable of tightly regulating a range of biological processes (ie, innate immunity, inflammation, and coagulation) through dynamic changes in its composition of the brush structure. Evaluating the specific roles of the endothelial glycocalyx under a range of pathophysiologic conditions has been a challenge in vitro as it is difficult to generate functional glycocalyces using commonly employed 2D cell culture models. We present a new multi-height microfluidic platform that promotes the growth of functional glycocalyces by eliciting unique shear stress forces over a continuous human umbilical vein endothelial cell monolayer at magnitudes that recapitulate the physical environment in arterial, capillary and venous regions of the vasculature. Following 72 hours of shear stress, unique glycocalyx structures formed within each region that were distinct from that observed in short (3 days) and long-term (21 days) static cell culture. The model demonstrated glycocalyx-specific properties that match the characteristics of the endothelium in arteries, capillaries and veins, with respect to surface protein expression, platelet adhesion, lymphocyte binding and nanoparticle uptake. With artery-to-capillary-to-vein transition on a 2 of 14 | SIREN Et al.
Background: Status epilepticus (SE) has traditionally been thought to cause cerebrospinal fluid (CSF) pleocytosis. However, attributing CSF pleocytosis solely to SE without addressing the underlying etiology may lead to poor outcomes. Leukocyte recruitment to CSF has been shown to peak around 24 hours after prolonged seizures in animal studies, suggesting that CSF pleocytosis within the first 24 hours of SE onset may be due to underlying causes. The goal of this study is to assess if SE is associated with CSF pleocytosis, independent of other causes within the first 24 hours of onset. Methods: We completed a historical cohort study of adult patients with SE admitted to the intensive care unit of Vancouver General Hospital between March 2010 and May 2019. Results: Of the 441 patients admitted with SE during the study period, 107 met our inclusion criteria leading to 111 lumbar punctures (LPs), with 4 patients receiving two LPs. CSF pleocytosis was seen in 12 of 72 patients who underwent an LP within the first 24 hours of SE onset. In all 12 patients, a secondary etiology for the pleocytosis was observed aside from SE. Of the six CSF samples collected after 24 hours of onset that demonstrated pleocytosis, four had no cause for pleocytosis other than SE. Conclusions: In all 12 patients with CSF pleocytosis in the first 24 hours of onset of SE, an underlying etiology was identified. Therefore, any pleocytosis noticed within the first 24 hours of onset of refractory SE should not be attributed solely to SE.
Background Lesser degrees of perioperative ischemia–reperfusion injury that does not require dialysis may nonetheless influence allograft outcomes, necessitating evaluation of suitable surrogate indicators of perioperative allograft injury. Methods This retrospective analysis of pediatric kidney transplants evaluated two indicators representing pace and completeness of recovery, for association with 12‐month estimated glomerular filtration rate (eGFR) and first‐year rate of eGFR decline: time to creatinine nadir (TTN) and ratio of recipient/donor unadjusted GFR (uGFRR/D) at 1‐month post‐transplant. Donor, recipient, and perioperative risk factors were tested further for association with these 2 indicators. Results 179 patients (190 transplants) aged 13 (IQR 7–17) years and 56% male were included. Twelve‐month eGFR was strongly associated with unadjusted GFR at 1 month (uGFR1M, p < .001) and uGFRR/D (p = .003), but not with TTN. None of the indicators was associated with the rate of subsequent eGFR decline after 1‐month post‐transplant. As a potential surrogate indicator, uGFR1M is effectively modeled by TTN and uGFRR/D (adjusted R2 = 0.57) and is associated with 12‐month eGFR (β = 0.81 ± 0.08; p < .001). Clinical factors associated with uGFRR/D included donor uGFR (p < .001), BSA (p = .026), age (p = .074), and recipient BSA (p < .001). Factors associated with pace of recovery (TTN) included donor uGFR (p = .018), type (p = .019), and recipient BSA (p = .022). Conclusions The uGFRR/D ratio, but not TTN, is a useful indicator of perioperative allograft damage that is associated with one‐year functional outcome; and uGFR1M is a potential early surrogate outcome. Donor, recipient, and perioperative factors that are associated with slow allograft function are identified.
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