Parents' and caregivers' experiences and behaviours when eating out with children with a food hypersensitivity.

BACKGROUND: For parents and caregivers of food hypersensitive (FH) children, accommodating their child's dietary needs when eating out can be a challenging experience. This study explored caregivers' experiences and behaviours when eating out with their FH child in order to gain insights into how they support and prepare their child in negotiating safe eating out experiences. METHODS: A cross-sectional, qualitative design was used. In depth, semi-structured interviews were carried out with 15 caregivers of children with FH. Interviews were analysed using framework analysis. RESULTS: Caregivers reported a number of issues relating to eating out with their FH child, or allowing their child to eat out without their supervision. Through themes of 'family context', 'child-focused concerns', and 'venue issues', caregivers described how they managed these and explained the limitations and sacrifices that FH imposed on their child, themselves, and family members. CONCLUSIONS: Through deeper understanding of the anxieties, negotiations and compromises experienced by caregivers of children with FH when they are eating out, clinicians and support charities can tailor their support to meet the needs of caregivers and children. Support and education provision should focus on providing caregivers of children with FH the tools and strategies to help enable safe eating out experiences.

Determinants of R-loop formation at convergent bidirectionally transcribed trinucleotide repeats.

R-loops have been described at immunoglobulin class switch sequences, prokaryotic and mitochondrial replication origins, and disease-associated (CAG)n and (GAA)n trinucleotide repeats. The determinants of trinucleotide R-loop formation are unclear. Trinucleotide repeat expansions cause diseases including DM1 (CTG)n, SCA1 (CAG)n, FRAXA (CGG)n, FRAXE (CCG)n and FRDA (GAA)n. Bidirectional convergent transcription across these disease repeats can occur. We find R-loops formed when CTG or CGG and their complementary strands CAG or CCG were transcribed; GAA transcription, but not TTC, yielded R-loops. R-loop formation was sensitive to DNA supercoiling, repeat length, insensitive to repeat interruptions, and formed by extension of RNA:DNA hybrids in the RNA polymerase. R-loops arose by transcription in one direction followed by transcription in the opposite direction, and during simultaneous convergent bidirectional transcription of the same repeat forming double R-loop structures. Since each transcribed disease repeat formed R-loops suggests they may have biological functions.

Familial gastric cancer - aetiology and pathogenesis.

Gastric cancer is the second most common cause of cancer death worldwide. It is estimated that 5-10% of gastric cancer cases have a familial association; however, knowledge concerning the genetic predisposition to familial gastric cancer is currently limited. In this chapter we discuss what is known about the aetiology and pathogenesis of both the diffuse and intestinal forms of familial gastric cancer. We focus particularly on hereditary diffuse gastric cancer because the discovery of germ-line E-cadherin mutations in a number of affected families has opened the prospect of identifying gene carriers, with implications for clinical management. The interplay of other conventional risk factors, such as Helicobacter pylori infection, with genetic factors is also discussed. It is hoped that understanding the genetic basis for familial gastric cancer will facilitate the development of clinically useful screening and preventative procedures.