Quantitative insights on de/repolymerization and deoxygenation of lignin in subcritical water.

The objective of the study was to investigate alkali lignin polymerization/depolymerization pathways in subcritical water (SW) without additives. Following a SW treatment at 200, 250, 275 and 300 °C, the products were subjected to a comprehensive suite of analyses addressing the product speciation and molecular weight (MW) distribution. The MW reduction (1.

Simple and sensitive dilute-and-shoot analysis of carotenoids in human plasma.

Carotenoids in human plasma are used as biomarkers of vegetable and fruit intake. Large sample volumes and intensive sample processing make measurement of these species cumbersome. We developed a dilute-and-shoot method for the quantitation of α-carotene, β-carotene, β-cryptoxanthin, lycopene and lutein/zeaxanthin using 10 μL of plasma.

Biodegradation of lignin by fungi, bacteria and laccases.

Indulin AT biodegradation by basidiomycetous fungi, actinobacteria and commercial laccases was evaluated using a suite of chemical analysis methods. The extent of microbial degradation was confirmed by novel thermal carbon analysis (TCA), as the treatments altered the carbon desorption and pyrolysis temperature profiles in supernatants. Laccase treatments caused only minor changes, though with increases occurring in the 850°C and char precursor fractions.

Improving clinical cognitive testing: report of the AAN Behavioral Neurology Section Workgroup.

Objective: To evaluate the evidence basis of single-domain cognitive tests frequently used by behavioral neurologists in an effort to improve the quality of clinical cognitive assessment.

Methods: Behavioral Neurology Section members of the American Academy of Neurology were surveyed about how they conduct clinical cognitive testing, with a particular focus on the Neurobehavioral Status Exam (NBSE). In contrast to general screening cognitive tests, an NBSE consists of tests of individual cognitive domains (e.

Pelizaeus-Merzbacher syndrome: neurocognitive function in a family with carrier manifestations.

A Cajun kindred with Pelizaeus-Merzbacher disease was found to have a p.Q128X mutation in exon 3B of proteolipid protein 1 (PLP1). The affected males were globally delayed in development, nonambulatory, and severely dysarthric.