Albumin and multiple sclerosis

A grant from the One-University Open Access Fund at the University of Kansas was used to defray the author's publication fees in this Open Access journal. The Open Access Fund, administered by librarians from the KU, KU Law, and KUMC libraries, is made possible by contributions from the offices of KU Provost, KU Vice Chancellor for Research & Graduate Studies, and KUMC Vice Chancellor for Research. For more information about the Open Access Fund, please see http://library.kumc.edu/authors-fund.xml.Leakage of the blood–brain barrier (BBB) is a common pathological feature in multiple sclerosis (MS). Following a breach of the BBB, albumin, the most abundant protein in plasma, gains access to CNS tissue where it is exposed to an inflammatory milieu and tissue damage, e.g., demyelination. Once in the CNS, albumin can participate in protective mechanisms. For example, due to its high concentration and molecular properties, albumin becomes a target for oxidation and nitration reactions. Furthermore, albumin binds metals and heme thereby limiting their ability to produce reactive oxygen and reactive nitrogen species. Albumin also has the potential to worsen disease. Similar to pathogenic processes that occur during epilepsy, extravasated albumin could induce the expression of proinflammatory cytokines and affect the ability of astrocytes to maintain potassium homeostasis thereby possibly making neurons more vulnerable to glutamate exicitotoxicity, which is thought to be a pathogenic mechanism in MS. The albumin quotient, albumin in cerebrospinal fluid (CSF)/albumin in serum, is used as a measure of blood-CSF barrier dysfunction in MS, but it may be inaccurate since albumin levels in the CSF can be influenced by multiple factors including: 1) albumin becomes proteolytically cleaved during disease, 2) extravasated albumin is taken up by macrophages, microglia, and astrocytes, and 3) the location of BBB damage affects the entry of extravasated albumin into ventricular CSF. A discussion of the roles that albumin performs during MS is put forth

Parent perceptions of early prognostic encounters following children’s severe traumatic brain injury: ‘Locked up in this cage of absolute horror’

OBJECTIVE: Little guidance exists for discussing prognosis in early acute care with parents following children’s severe traumatic brain injury (TBI). Providers’ beliefs about truth-telling can shape what is said, how it is said, and how providers respond to parents. METHODS: This study was part of a large qualitative study conducted in the USA (42 parents/37 families) following children’s moderate to severe TBI (2005 to 2007). Ethnography of speaking was used to analyse interviews describing early acute care following children’s severe TBI (29 parents/25 families). RESULTS: Parents perceived that: a) parents were disadvantaged by provider delivery; b) negative outcome values dominated some provider’s talk; c) truth-telling involves providers acknowledging all possibilities; d) framing the child’s prognosis with negative medical certainty when there is some uncertainty could damage parent-provider relationships; e) parents needed to remain optimistic; and, f) children’s outcomes could differ from providers’ early acute care prognostications. CONCLUSION: Parents blatantly and tacitly revealed their beliefs that providers play an important role in shaping parent reception of and synthesis of prognostic information, which constructs the family’s ability to cope and participate in shared decision-making. Negative medical certainty created a fearful or threatening environment that kept parents from being fully informed