Comment on "Wandering minds: the default network and stimulus-independent thought"

Mason et al. (Reports, 19 January 2007, p. 393) attributed activity in certain regions of the "resting" brain to the occurrence of mind-wandering. However, previous research has demonstrated the difficulty of distinguishing this type of stimulus-independent thought from stimulus-oriented thought (e.g., watchfulness). Consideration of both possibilities is required to resolve this ambiguity.     

Evaluation of the Biochemical Components and Chromatic Properties of the Juice of <Emphasis Type="Italic">Vaccinium macrocarpon</Emphasis> Aiton and <Emphasis Type="Italic">Vaccinium oxycoccos</Emphasis> L.

Benzoic acid, total anthocyanins, soluble solids, titratable acidity, and colour properties in juice of the American cranberry Vaccinium macrocarpon and the European cranberry Vaccinium oxycoccos were investigated. Berry juices of V. macrocarpon cultivars were distinguished by their higher total anthocyanin and benzoic acid amounts. These cultivars accumulated on average 43.11 mg/l of benzoic acid and 92.45 mg/l of total anthocyanins. The levels of benzoic acid and total anthocyanins in V. oxycoccos cultivars were 17.52 mg/l and 42.54 mg/l, respectively. The V. macrocarpon cultivars ‘Franklin’, ‘Le Munyon’, ‘Searles’, and ‘Early Richard’ were selected as the best according to the enhanced total anthocyanins and benzoic acid amounts. The separation of anthocyanins by HPLC-UV-VIS revealed the presence of six anthocyanins, with peonidin-3-galactoside being the most prevalent. Galactoside together with glucoside conjugates comprised the largest percentage of total anthocyanins in the juices of V. macrocarpon and V. oxycoccos cultivars.     

The use of non-prion biomarkers for the diagnosis of Transmissible Spongiform Encephalopathies in the live animal

Scrapie and bovine spongiform encephalopathy (BSE) are major global concerns and the emergence of variant Creutzfeldt-Jakob disease (vCJD) has caused turmoil for blood transfusion services and hospitals worldwide. Recent reports of iatrogenic CJD (iCJD) cases following blood transfusions from Transmissible Spongiform Encephalopathies (TSE)-infected donors have fuelled this concern. Major diagnostic tests for BSE and scrapie are conducted post-mortem from animals in late stages of the disease. Although the lymphoreticular system is involved in the earlier pathogenesis of some forms of sheep scrapie and vCJD, which presents great opportunity for diagnostic development, other TSE diseases (some strains of scrapie, sporadic CJD (sCJD) and bovine BSE) do not present such a diagnostic opportunity. Thus, there is an urgent need for pre-mortem tests that differentiate between healthy and diseased individuals at early stages of illness, in accessible samples such as blood and urine using less invasive procedures. This review reports on the current state of progress in the development and use of prion and non-prion biomarkers in the diagnosis of TSE diseases. Some of these efforts have concentrated on improving the sensitivity of PrPSc detection to allow in vivo diagnosis at low abundances of PrPSc whilst others have sought to identify non-prion protein biomarkers of TSE disease, many of which are still at early stages of development. In this review we comment upon the limitations of prion based tests and review current research on the development of tests for TSE that rely on non-prion disease markers in body fluids that may allow preclinical disease diagnosis.     

Activating mutations of NOTCH1 in human T cell acute lymphoblastic leukemia

Very rare cases of human T cell acute lymphoblastic leukemia (T-ALL) harbor chromosomal translocations that involve NOTCH1, a gene encoding a transmembrane receptor that regulates normal T cell development. Here, we report that more than 50% of human T-ALLs, including tumors from all major molecular oncogenic subtypes, have activating mutations that involve the extracellular heterodimerization domain and/or the C-terminal PEST domain of NOTCH1. These findings greatly expand the role of activated NOTCH1 in the molecular pathogenesis of human T-ALL and provide a strong rationale for targeted therapies that interfere with NOTCH signaling.