Transcriptome analysis of genetically matched human induced pluripotent stem cells disomic or trisomic for chromosome 21.

Trisomy of chromosome 21, the genetic cause of Down syndrome, has the potential to alter expression of genes on chromosome 21, as well as other locations throughout the genome. These transcriptome changes are likely to underlie the Down syndrome clinical phenotypes. We have employed RNA-seq to undertake an in-depth analysis of transcriptome changes resulting from trisomy of chromosome 21, using induced pluripotent stem cells (iPSCs) derived from a single individual with Down syndrome.

Maternity perception by pregnant women living with HIV.

Objective: Identify the perceptions of pregnant women living with HIV about motherhood and understand the expectations and feelings experienced by these women.

Methodology: Study with descriptive design and qualitative approach, carried out with 10 pregnant women living with HIV who attend the prenatal service of a university hospital in Rio de Janeiro, Brazil. The participants answered a semi-structured interview.

Multi-tier regulation of the streptomycete morphogenetic peptide SapB.

Streptomyces coelicolor is a morphologically complex bacterium requiring the secretion of surface-active proteins to progress through its life cycle. SapB represents an important class of these biosurfactants, as illustrated by its ability to restore aerial hyphae formation when applied exogenously to developmental mutants. However, such aerial hyphae fail to sporulate, exemplifying the need to co-ordinate the timing of SapB production with other developmental events.

A glycine zipper motif mediates the formation of toxic β-amyloid oligomers in vitro and in vivo.

Background: The β-amyloid peptide (Aβ) contains a Gly-XXX-Gly-XXX-Gly motif in its C-terminal region that has been proposed to form a "glycine zipper" that drives the formation of toxic Aβ oligomers. We have tested this hypothesis by examining the toxicity of Aβ variants containing substitutions in this motif using a neuronal cell line, primary neurons, and a transgenic C. elegans model.

AIP-1 ameliorates beta-amyloid peptide toxicity in a Caenorhabditis elegans Alzheimer's disease model.

Multiple neurodegenerative diseases are causally linked to aggregation-prone proteins. Cellular mechanisms involving protein turnover may be key defense mechanisms against aggregating protein disorders. We have used a transgenic Caenorhabditis elegans Alzheimer's disease model to identify cellular responses to proteotoxicity resulting from expression of the human beta amyloid peptide (Abeta).