Release Kinetics of Dexamethasone Phosphate from Porous Chitosan: Comparison of Aerogels and Cryogels

International audiencePorous chitosan materials as potential wound dressings were prepared via dissolution of chitosan, nonsolvent-induced phase separation in NaOH-water, formation of a hydrogel, and either freeze-drying or supercritical CO2 drying, leading to "cryogels" and "aerogels", respectively. The hydrophilic drug dexamethasone sodium phosphate was loaded by impregnation of chitosan hydrogel, and the release from cryogel or aerogel was monitored at two pH values relevant for wound healing. The goal was to compare the drug-loading efficiency and release behavior from aerogels and cryogels as a function of the drying method, the materials' physicochemical properties (density, morphology), and the pH of the release medium. Cryogels exhibited a higher loading efficiency and a faster release in comparison with aerogels. A higher sample density and lower pH value of the release medium resulted in a more sustained release in the case of aerogels. In contrast, for cryogels, the density and pH of the release medium did not noticeably influence release kinetics. The Korsmeyer-Peppas model showed the best fit to describe the release from the porous chitosan materials into the different media

Cerebral Perfusion Pressure Variability Between Patients and Between Centres

 The aim of this analysis was to investigate to what extent median cerebral perfusion pressure (CPP) differs between severe traumatic brain injury (TBI) patients and between centres, and whether the 2007 change in CPP threshold in the Brain Trauma Foundation guidelines is reflected in patient data collected at several centres over different time periods.status: publishe

Acute Serum Hormone Levels: Characterization and Prognosis after Severe Traumatic Brain Injury

Experimental traumatic brain injury (TBI) studies report the neuroprotective effects of female sex steroids on multiple mechanisms of injury, with the clinical assumption that women have hormonally mediated neuroprotection because of the endogenous presence of these hormones. Other literature indicates that testosterone may exacerbate injury. Further, stress hormone abnormalities that accompany critical illness may both amplify or blunt sex steroid levels. To better understand the role of sex steroid exposure in mediating TBI, we 1) characterized temporal profiles of serum gonadal and stress hormones in a population with severe TBI during the acute phases of their injury; and 2) used a biological systems approach to evaluate these hormones as biomarkers predicting global outcome. The study population was 117 adults (28 women; 89 men) with severe TBI. Serum samples (n=536) were collected for 7 days post-TBI for cortisol, progesterone, testosterone, estradiol, luteinizing hormone (LH), and follicle-stimulating hormone (FSH). Hormone data were linked with clinical data, including acute care mortality and Glasgow Outcome Scale (GOS) scores at 6 months. Hormone levels after TBI were compared to those in healthy controls (n=14). Group based trajectory analysis (TRAJ) was used to develop temporal hormone profiles that delineate distinct subpopulations in the cohort. Structural equations models were used to determine inter-relationships between hormones and outcomes within a multivariate model. Compared to controls, acute serum hormone levels were significantly altered after severe TBI. Changes in the post-TBI adrenal response and peripheral aromatization influenced hormone TRAJ profiles and contributed to the abnormalities, including increased estradiol in men and increased testosterone in women. In addition to older age and greater injury severity, increased estradiol and testosterone levels over time were associated with increased mortality and worse global outcome for both men and women. These findings represent a paradigm shift when thinking about the role of sex steroids in neuroprotection clinically after TBI