Proposing and evaluating a model of depression, stress, resilience and spirituality in relation to pain in women with breast cancer: Investigating the mediating role of mindfulness.

BACKGROUND: Pain experience is one of the most common symptoms of women with breast cancer receiving chemotherapy. It may cause physical and psychological problems and interfere with the treatment process. AIMS: This study aimed to examine the relationship between depression, stress, resilience and spirituality on the pain symptoms of breast cancer patients during chemotherapy and explore the potential mediating role of mindfulness in this association. METHOD: Two hundred and forty women with breast cancer receiving chemotherapy from Shiraz University Hospital, were selected and evaluated by a purposive sampling method. The research instruments were Perceived Stress Scale, Beck Depression Questionnaire-2, Mindfulness, Resilience, Spirituality and Pain Questionnaires. The obtained data was analyzed by SPSS software and MPLUS using Spearman correlation coefficient and path analysis. RESULTS: Based on the findings of direct path analysis, depression, stress, and spirituality showed a significant relationship with mindfulness, but resilience had no significant relationship with mindfulness (p < 0.01). Furthermore, depression, stress, resilience, and mindfulness showed a significant relationship with pain, while spirituality had no significant relationship with pain (p < 0.01). Finally, indirect path analysis revealed mindfulness is a significant mediator of stress and pain (p < 0.05). CONCLUSIONS: The present study suggested a model can be useful in better understanding of the psychological components affecting pain in breast cancer patients, after and during their treatments. It also provided an effective framework to develop and investigate pain-focused and non-pharmacological interventions.

BDNF (rs6265) Val < Met polymorphism can buffer cognitive functions against post stroke CT/MRI pathological findings.

Brain lesions following stroke have been shown prevalently in CT/MRI, and it was confirmed that lesions usually are accompanied by cognitive deficits. Although previous studies have emphasized that BDNF Val66Met polymorphism had a substantial role in neurogenesis and synaptic plasticity, it remains unclear to what extent an interaction may be appeared between neuroimaging findings and Val66Met variants on different cognitive functions following stroke. In a case-control study the carriers of at least one Val allele (n = 56), were compared with the carriers of Met/Met homozygotes (n = 156) in order to find possible neuroimaging factors in relation to cognitive functions in a sample from the north of Iran. The third edition of Addenbrooke's Cognitive Examination (ACE-III) was used to determine the cognitive functions. There were interactive effects among Val66Met genotypes with dominant hemisphere lesions [F = 6.97, ή2 = 0.03, p = 0.009], cerebral atrophy [F = 5.43, ή2 = 0.03, p = 0.011] and number of lesions [F = 4.32, ή2 = 0.04, p = 0.014], for visuospatial skills, memory, and attention functions respectively; implying that the effect of dominant hemisphere lesions, cerebral atrophy, and multiple lesions on cognitive functions have been modulated by Met/Met homozygosity. The destructive effect of Val/Met homozygosity on cognitive functions was shown to be exacerbated by dominant hemispheric lesions, cerebral atrophy, and multiple lesions following stroke. The findings of present research support our hypothesis that interaction of Val66Met variants with cerebral lesions is associated with cognitive dysfunctions in post stroke conditions; particularly through Met/Met homozygosity which act as a buffer mechanism against some CT/MRI pathological findings.

Brain-derived neurotrophic factor (BDNF) Val66Met polymorphism and post-stroke dementia: a hospital-based study from northern Iran.

Brain-derived neurotrophic factor (BDNF) Val66Met polymorphism is associated with functional and cognitive outcomes of stroke and plays a key role in preventing neuronal death. This study aimed to answer the following question: does BDNF Val66Met polymorphism prognosticate survival status and risk of post-stroke dementia (PSD)? In a retrospective cohort study, 206 patients with ischemic stroke (IS) entered the study. They were consecutively being admitted to the neurology clinic in Poursina Hospital (northern Iran) from 2012 to 2014. The diagnosis of PSD was based on DSM-5 criteria. The current and the premorbid cognitive statuses of the patients were respectively assessed through the third edition of Addenbrooke's Cognitive Examination and the Informant Questionnaire on Cognitive Decline in the Elderly. BDNF Val66Met gene polymorphism was determined by PCR-RFLP. On average, 48 patients (23.3 %) developed PSD 6 months after IS. Log-rank test showed that the survival rate of at least one Val-allele carriers was significantly lower than that of Met/Met homozygotes (P = 0.0005), and the former developed PSD sooner than the latter (375, 492 days, respectively). Cox model showed that heterozygous carriers of Val/Met were at greater risk of PSD over time (HR 2.280, 95 % CI 1.566-4.106, P = 0.006). However, the risk ratio of patients with PSD among different BDNF genotypes decreased after adjusting demographic, clinical, and vascular risk factors, and was no longer statistically significant (AHR 2.434, 95 % CI 0.597-9.926, P = 0.215). Val-allele carriers or Val/Met genotypes were more quickly diagnosed as having dementia after IS. However, this genetic vulnerability became more destructive when it was added to demographic, clinical, and vascular risk factors.