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Biomedical subjects

Angela Freeman

Publications and source records attributed to Angela Freeman.

4 recordsLinked to original sources
PubMed2004

Improving the diet of toddlers of Pakistani origin: a study of intensive dietary health education.

OBJECTIVE: To determine whether an intensive, home-based programme of dietary health education resulted in improved maternal knowledge and changes in toddlers' diets in families of Pakistani origin. DESIGN: Prospective intervention study. SETTING AND PARTICIPANTS: The study took place in Keighley, West Yorkshire, England. Thirty-three mothers, whose toddlers had been found to be anaemic, entered the programme; 26 completed it. Dietary health education was delivered by a trained link worker, supported by health visitors, a dietitian and a community paediatrician. INTERVENTION: Six one-hour visits were made at weekly intervals. The teaching programme focused on healthy weaning, with an emphasis on adequate intake of iron-rich foods. A purpose-designed pictorial teaching aid was used. OUTCOME MEASURES: Maternal knowledge was assessed by targeted questions. Children's diets were assessed using 24-hour dietary recall and weekly food frequency, from which a "food frequency" score was derived. RESULTS: There were significant gains in maternal dietary knowledge. There were modest improvements in children's diets. The programme was valued by the mothers. CONCLUSIONS: Mothers of Pakistani origin gained knowledge and changed their children's diets following the dietary health education programme. The study demonstrated the value of a home-based programme delivered by a trained link worker to this group, which has difficulty in accessing clinic-based services.

Anemia, Iron-Deficiency↗
PubMed2003

Phospholipid scramblase 3 controls mitochondrial structure, function, and apoptotic response.

Phospholipid scramblase 3 (PLS3) is a newly recognized member of a family of proteins responsible for phospholipid translocation between two lipid compartments. To study PLS3 function in mitochondria, we disrupted its conserved calcium-binding motif yielding an inactive mutant PLS3(F258V). Cells transfected with PLS3(F258V) exhibited reduced proliferative capacity. Mitochondrial analysis revealed that PLS3(F258V)-expressing cells have decreased mitochondrial mass shown by lower cytochrome c and cardiolipin (CL) content, poor mitochondrial respiration, and reduced oxygen consumption and intracellular ATP; whereas wild-type PLS3-transfected cells exhibit increased mitochondrial mass and enhanced respiration. Electron microscopic examination revealed that the mitochondria in PLS3(F258V)-expressing cells have densely packed cristae and are fewer in number and larger than those in control cells. The abnormal mitochondrial metabolism and structure in PLS3(F258V)-expressing cells were associated with decreased sensitivity to UV- and tBid-induced apoptosis and diminished translocation of CL to the mitochondrial outer membrane. In contrast, wild-type PLS3-transfected cells displayed increased sensitivity to apoptosis and enhanced CL translocation. These studies identify PLS3 as a critical regulator of mitochondrial structure and respiration, and CL transport in apoptosis.

Apoptosis↗
PubMed2002

The apoptotic effect of HA14-1, a Bcl-2-interacting small molecular compound, requires Bax translocation and is enhanced by PK11195.

HA14-1 is a small molecular compound that was identified based on the structure of Bcl-2. HA14-1 interacts with Bcl-2 and inhibits the antiapoptotic effect of Bcl-2. We investigated the mechanism of HA14-1-induced apoptosis and found that HA14-1 induces translocation of Bax from cytosols to the mitochondria. Cells deficient in Bax were much more resistant to HA14-1-induced apoptosis, suggesting that Bax is required for this process. A pan-caspase inhibitor failed to inhibit the apoptotic effect of HA14-1, indicating that this is through a caspase-independent pathway. To eliminate the effect of cytosolic Bax, we incubated cell-free mitochondria with HA14-1 to study its effect on cytochrome c release. HA14-1 was ineffective in causing cytochrome c release from the purified mitochondria. However, the combination of HA14-1 and PK11195, an antagonist of peripheral benzodiazepine receptor of the mitochondria, enhanced the cytochrome c release by HA14-1. The combination of PK11195 and HA14-1 could therefore serve as a potentially useful approach to enhance apoptosis in cancer.

Animals↗