Unmet needs and health-related quality of life of breast cancer survivors: survey from Gaza Strip, Palestine.

BACKGROUND: Cancer, especially breast cancer, remains a public health problem because of its negative consequences, which require long-term programs to alleviate its devastating effects. This study aimed to examine unmet supportive care needs and health-related quality of life of females with breast cancer. METHODS: A cross-sectional study with a mixed-method design was employed. A simple, randomly selected sample of 352 females attending Al-Rantisi and Al-Amal hospitals was included in this study. A validated Arabic version of the Supportive Care Needs Survey (34 items) and The European Organization for Research and Treatment of Cancer Quality of Life (EORTC QLQ-C15-PAL) were used. Moreover, twenty-five semi-structured interviews were performed (13 females, eight husbands, and four healthcare workers). Quantitative data were analysed using descriptive and inferential analysis, whereas thematic analysis was used for qualitative data to highlight main themes. RESULTS: The highest unmet need reported by females with breast cancer was psychological needs (63%), followed by health-related systems and information (62%) and physical and daily life (61%). Pain and fatigue were the most reported symptoms (65.8% and 62.5%, respectively), followed by emotional distress, physical function, and physical symptoms; 55.8%, 54.3%, and 51.5%, respectively. These unmet needs and health-related quality of life-related dimensions were highlighted and elicited by qualitative data analysis. Unmet needs are high among married females, on conservative treatments, young females (< 40 years old), and females in the first year of diagnosis. The presence of chronic diseases did not increase needs. However, health-related quality of life was affected. Six themes are subtracted: availability of anticancer therapy, affordability of healthcare, family and social support, psychological support, health education, and self-image & intimate relationship. CONCLUSION: Many needs are unmet. Caring for females with breast cancer should be comprehensive to fill gaps, including psychological care, health information and education, physical care and support, and medical care.

Metal-dependent generation of reactive oxygen species from amyloid proteins implicated in neurodegenerative disease.

Using a method based on ESR spectroscopy and spin-trapping, we have shown that Abeta (amyloid beta-peptide) (implicated in Alzheimer's disease), alpha-synuclein (implicated in Parkinson's disease), ABri (British dementia peptide) (responsible for familial British dementia), certain toxic fragments of the prion protein (implicated in the transmissible spongiform encephalopathies) and the amylin peptide (found in the pancreas in Type 2 diabetes mellitus) all have the common ability to generate H(2)O(2) in vitro. Numerous controls (reverse, scrambled and non-toxic peptides) lacked this property. We have also noted a positive correlation between the ability of the various proteins tested to generate H(2)O(2) and their toxic effects on cultured cells. In the case of Abeta and ABri, we have shown that H(2)O(2) is generated as a short burst during the early stages of aggregation and is associated with the presence of protofibrils or oligomers, rather than mature fibrils. H(2)O(2) is readily converted into the aggressive hydroxyl radical by Fenton chemistry, and this extremely reactive radical could be responsible for much of the oxidative damage seen in all of the above disorders. We suggest that the formation of a redox-active complex involving the relevant amyloidogenic protein and certain transition-metal ions could play an important role in the pathogenesis of several different protein misfolding disorders.

Copper-mediated formation of hydrogen peroxide from the amylin peptide: a novel mechanism for degeneration of islet cells in type-2 diabetes mellitus?

Amyloid deposits derived from the amylin peptide accumulate within pancreatic islet beta-cells in most cases of type-2 diabetes mellitus (T2Dm). Human amylin 'oligomers' are toxic to these cells. Using two different experimental techniques, we found that H(2)O(2) was generated during the aggregation of human amylin into amyloid fibrils. This process was greatly stimulated by Cu(II) ions, and human amylin was retained on a copper affinity column. In contrast, rodent amylin, which is not toxic, failed to generate any H(2)O(2) and did not interact with copper. We conclude that the formation of H(2)O(2) from amylin could contribute to the progressive degeneration of islet cells in T2Dm.

The amylin peptide implicated in type 2 diabetes stimulates copper-mediated carbonyl group and ascorbate radical formation.

Human amylin (hA), which is toxic to islet ß-cells, can self-generate H(2)O(2), and this process is greatly enhanced in the presence of Cu(II) ions. Here we show that carbonyl groups, a marker of oxidative modification, were formed in hA incubated in the presence of Cu(II) ions or Cu(II) ions plus H(2)O(2), but not in the presence of H(2)O(2) alone. Furthermore, under similar conditions (i.e., in the presence of both Cu(II) ions and H(2)O(2)), hA also stimulated ascorbate radical formation. The same observations concerning carbonyl group formation were made when the histidine residue (at position 18) in hA was replaced by alanine, indicating that this residue does not play a key role. In complete contrast to hA, rodent amylin, which is nontoxic, does not generate H(2)O(2), and binds Cu(II) ions only weakly, showed none of these properties. We conclude that the hA-Cu(II)/Cu(I) complex is redox active, with electron donation from the peptide reducing the oxidation state of the copper ions. The complex is capable of forming H(2)O(2) from O(2) and can also generate (•)OH via Fenton chemistry. These redox properties of hA can explain its ability to stimulate copper-mediated carbonyl group and ascorbate radical formation. The formation of reactive oxygen species from hA in this way could hold the key to a better understanding of the damaging consequences of amyloid formation within the pancreatic islets of patients with type 2 diabetes mellitus.