The effects of acute alcohol intake on endogenous vs. exogenous attention in visual perception.

Acute alcohol consumption is known to impair visual perception, yet the underlying mechanisms remain poorly understood. Visual perception is influenced by visual attention, which comprises two distinct components: endogenous (voluntary) and exogenous (involuntary) attention. This study investigated how a moderate alcohol dose alters attentional modulation of visual perception.

Germline PIK3CA and AKT1 mutations in Cowden and Cowden-like syndromes.

Cowden syndrome (CS) is a difficult-to-recognize multiple hamartoma syndrome with high risks of breast, thyroid, and other cancers. Germline mutations in PTEN on 10q23 were found to cause 85% of CS when accrued from tertiary academic centers, but prospective accrual from the community over the last 12 years has revealed a 25% PTEN mutation frequency. PTEN is the phosphatase that has been implicated in a heritable cancer syndrome and subsequently in multiple sporadic cancers and developmental processes.

Abnormal brain iron homeostasis in human and animal prion disorders.

Neurotoxicity in all prion disorders is believed to result from the accumulation of PrP-scrapie (PrP(Sc)), a beta-sheet rich isoform of a normal cell-surface glycoprotein, the prion protein (PrP(C)). Limited reports suggest imbalance of brain iron homeostasis as a significant associated cause of neurotoxicity in prion-infected cell and mouse models. However, systematic studies on the generality of this phenomenon and the underlying mechanism(s) leading to iron dyshomeostasis in diseased brains are lacking.

Evaluation of the human transmission risk of an atypical bovine spongiform encephalopathy prion strain.

Bovine spongiform encephalopathy (BSE), the prion disease in cattle, was widely believed to be caused by only one strain, BSE-C. BSE-C causes the fatal prion disease named new variant Creutzfeldt-Jacob disease in humans. Two atypical BSE strains, bovine amyloidotic spongiform encephalopathy (BASE, also named BSE-L) and BSE-H, have been discovered in several countries since 2004; their transmissibility and phenotypes in humans are unknown.