Infant and Young Child Feeding Counseling, Decision-Making, and Practices Among HIV-Infected Women in Malawi’s Option B+ Prevention of Mother-to-Child Transmission Program: A Mixed Methods Study

This study examined infant and young child feeding (IYCF) counseling, decision-making, and practices among HIV-infected women with children 0–23 months participating in Malawi’s Option B+ prevention of mother-to-child transmission (PMTCT) program. We conducted 160 survey interviews, 32 in-depth interviews, and 32 observations of PMTCT visits. Surveys indicated that exclusive breastfeeding was common (75%) among children < 6 months, while minimum dietary diversity (41%) and minimum acceptable diet (40%) for children 6–23 months occurred less often. In-depth interviews supported these findings. Most women felt comfortable with current breastfeeding recommendations, but chronic food insecurity made it difficult for them to follow complementary feeding guidelines. Women trusted IYCF advice from health workers, but mainly received it during pregnancy. During observations of postnatal PMTCT visits, health workers infrequently advised on breastfeeding (41% of visits) or complementary feeding (29% of visits). This represents a missed opportunity for health workers to support optimal IYCF practices within Option B+

Polyglutamine disruption of the huntingtin exon 1 N terminus triggers a complex aggregation mechanism

Simple polyglutamine (polyQ) peptides aggregate in vitro via a nucleated growth pathway directly yielding amyloid-like aggregates. We show here that the 17 amino acid flanking sequence (httNT) N-terminal to the polyQ in the toxic huntingtin exon1 fragment imparts onto this peptide a complex alternative aggregation mechanism. In isolation the httNT peptide is a compact coil that resists aggregation. When polyQ is fused to this sequence, it induces in httNT, in a repeat-length dependent fashion, a more extended conformation that greatly enhances its aggregation into globular oligomers with httNT cores and exposed polyQ. In a second step, a new, amyloid-like aggregate is formed with a core composed of both httNT and polyQ. The results indicate unprecedented complexity in how primary sequence controls aggregation within a substantially disordered peptide, and have implications for the molecular mechanism of Huntington&apos;s disease. There are nine known expanded CAG repeat diseases, in which expansion of a disease protein&apos;s polyglutamine (polyQ) sequence beyond a threshold repeat length causes progressive neurodegeneration through a predominantly gain-of-function mechanism 1. In Huntington&apos;s disease (HD) the repeat length threshold is about 37 glutamines 2. A majo