Life experiences and coping mechanisms among breast cancer patients in an urban Malaysian hospital : a qualitative study

Breast cancer is top-ranking cancer that affects the quality of life among women in Malaysia. Although it is very difficult to define the quality of life (QoL) precisely, it has a broad concept that affects global life satisfaction, which includes good health, adequate housing, employment, personal and family safety, interrelationships, education, and leisure pursuits. In this study, we aimed to discuss the life changes upon being diagnosed with breast cancer and their perception of social support. We also discussed the spirituality factor in patients’ coping mechanism with their health condition. This study was carried out using a purposive sampling method. The perception of social support, quality of life, and religiosity factor is discussed through the perspectives of nine breast cancer patients with an interview consisting of semi-structured questions. Basic interpretive qualitative methodology was applied to analyse the perception of social support and religiosity factor as a coping mechanism. The results showed that all the breast cancer patients reported good social support from family and friends except for one patient. Five themes were identified, namely patterns of life, supportive atmosphere, decision making and confidence, expectation, as well as psychological defences and spirituality. Seven out of nine patients reported that their religion helped them to cope with the disease by maintaining self-esteem, providing a sense of meaning and purpose, giving emotional comfort, and providing a sense of hope. In conclusion, social support and religious factor are very important in the lives of breast cancer patients in dealing with their health condition

Herpes simplex encephalitis is linked with selective mitochondrial damage; a post-mortem and in vitro study

Herpes simplex virus type-1 (HSV-1) encephalitis (HSE) is the most commonly diagnosed cause of viral encephalitis in western countries. Despite antiviral treatment, HSE remains a devastating disease with high morbidity and mortality. Improved understanding of pathogenesis may lead to more effective therapies. Mitochondrial damage has been reported during HSV infection in vitro. However, whether it occurs in the human brain and whether this contributes to the pathogenesis has not been fully explored. Minocycline, an antibiotic, has been reported to protect mitochondria and limit brain damage. Minocycline has not been studied in HSV infection. In the first genome-wide transcriptomic study of post-mortem human HSE brain tissue, we demonstrated a highly preferential reduction in mitochondrial genome (MtDNA) encoded transcripts in HSE cases (n = 3) compared to controls (n = 5). Brain tissue exhibited a significant inverse correlation for immunostaining between cytochrome c oxidase subunit 1 (CO1), a MtDNA encoded enzyme subunit, and HSV-1; with lower abundance for mitochondrial protein in regions where HSV-1 was abundant. Preferential loss of mitochondrial function, among MtDNA encoded components, was confirmed using an in vitro primary human astrocyte HSV-1 infection model. Dysfunction of cytochrome c oxidase (CO), a mitochondrial enzyme composed predominantly of MtDNA encoded subunits, preceded that of succinate dehydrogenase (composed entirely of nuclear encoded subunits). Minocycline treated astrocytes exhibited higher CO1 transcript abundance, sustained CO activity and cell viability compared to non-treated astrocytes. Based on observations from HSE patient tissue, this study highlights mitochondrial damage as a critical and early event during HSV-1 infection. We demonstrate minocycline preserves mitochondrial function and cell viability during HSV-1 infection. Minocycline, and mitochondrial protection, offers a novel adjunctive therapeutic approach for limiting brain cell damage and potentially improving outcome among HSE patients

Formation of eicosanoids, E2/D2 isoprostanes, and docosanoids following decapitation-induced ischemia, measured in high-energy-microwaved rat brain*

Inflammatory lipid mediators derived from arachidonic acid (AA) and docosahexaenoic acid (DHA) modify the pathophysiology of brain ischemia. The goal of this work was to investigate the formation of eicosanoids and docosanoids generated from AA and DHA, respectively, during no-flow cerebral ischemia. Rats were subjected to head-focused microwave irradiation 5 min following decapitation (complete ischemia) or prior to decapitation (controls). Brain lipids were extracted and analyzed by reverse-phase liquid chromatography-tandem mass spectrometry. After complete ischemia, brain AA, DHA, and docosapentaenoic acid concentrations increased 18-, 5- and 4-fold compared with controls, respectively. Prostaglandin E2 (PGE2) and PGD2 could not be detected in control microwaved rat brain, suggesting little endogenous PGE2/D2 production in the brain in the absence of experimental manipulation. Concentrations of thromboxane B2, E2/D2-isoprostanes, 5-hydroxyeicosatetraenoic acid (5-HETE), 5-oxo-eicosatetraenoic acid, and 12-HETE were significantly elevated in ischemic brains. In addition, DHA products such as mono-, di- and trihydroxy-DHA were detected in control and ischemic brains. Monohydroxy-DHA, identified as 17-hydroxy-DHA and thought to be the immediate precursor of neuroprotectin D1, was 6.5-fold higher in ischemic than in control brain. The present study demonstrated increased formation of eicosanoids, E2/D2-IsoPs, and docosanoids following cerebral ischemia. A balance of these lipid mediators may mediate immediate events of ischemic injury and recovery