Experiences of Fathers in Norway Attending an Online Course on Therapeutic Writing After the Death of a Child

After the unexpected death of a child, bereaved parents require prompt access to helpful support systems. Online therapeutic writing courses can make such support accessible. Because few studies have included bereaved fathers as participants, we explored the experiences of fathers whose children died unexpectedly and who were part of an online course of therapeutic writing in Norway. We piloted two courses (group 1, six weeks, n = 9; group 2, 5 weeks, n = 5). We describe our methodological considerations for using poetic representations in qualitative health research and present four poetic representations based on fieldwork notes written by the principal investigator. Then, we triangulate and narratively analyze them together with two collective poems written by participants from each group; excerpts of the writings from two fathers, one per group; evaluation surveys (n = 4; n = 3); and, anonymous check-out journaling from the second group (n = 3). Resistance was a salient feature of our participants’ grief, and writing enabled them to both be in contact with their emotional world and process difficult emotions as they looked for meaning despite the death of their children. Those who attended the most classes perceived the course as transformative, being part of an ongoing self-exploration, and a possibility to continue and strengthen the bond with their children. Our findings mirror the complexities of the grief experiences of fathers, giving account of their need to find a rhythm to dive into their emotional world, the importance of peer support, and the value of diversifying intervention techniques to meet individual needs and preferences.publishedVersio

Experiences of Norwegian Mothers Attending an Online Course of Therapeutic Writing Following the Unexpected Death of a Child

The unexpected death of a child is one of the most challenging losses as it fractures survivors’ sense of parenthood and other layers of identity. Given that not all the bereaved parents who have need for support respond well to available treatments and that many have little access to further intervention or follow-up over time, online interventions featuring therapeutic writing and peer support have strong potential. In this article we explore how a group of bereaved mothers experienced the process of participating in an online course in therapeutic writing for the integration of grief. Our research questions were: How do parents who have lost a child experience being part of an online course in therapeutic writing? What are the perceived benefits and challenges of writing in processing their grief? We followed an existential phenomenological approach and analyzed fieldwork notes (n = 13), qualitative data from the application and assessment surveys (n = 35; n = 21), excerpts from the journals of some participants (n = 3), and email correspondence with some participants (n = 5). We categorized the results in three meaning units: (1) where does my story begin? The “both and” of their silent chaos; (2) standing on the middle line: a pregnancy that does not end; (3) closures and openings: “careful optimism” and the need for community support. Participants experienced writing as an opportunity for self-exploration regarding their identities and their emotional world, as well as a means to develop and strengthen a bond with their children. They also experienced a sense of belonging, validation, and acceptance in the online group in a way that helped them make sense of their suffering. Online writing courses could be of benefit for bereaved parents who are grieving the unexpected death of a child, but do not replace other interventions such as psychotherapy. In addition to trauma and attachment informed models of grief, identity informed models with a developmental focus might enhance the impact of both low-threshold community interventions and more intensive clinical ones. Further studies and theoretical development in the area are needed, addressing dialogical notions such as the multivoicedness of the self.publishedVersio

High-resolution visualization and assessment of basal and OXPHOS-induced mitophagy in H9c2 cardiomyoblasts

Mitochondria are susceptible to damage resulting from their activity as energy providers. Damaged mitochondria can cause harm to the cell and thus mitochondria are subjected to elaborate quality-control mechanisms including elimination via lysosomal degradation in a process termed mitophagy. Basal mitophagy is a house-keeping mechanism fine-tuning the number of mitochondria according to the metabolic state of the cell. However, the molecular mechanisms underlying basal mitophagy remain largely elusive. In this study, we visualized and assessed the level of mitophagy in H9c2 cardiomyoblasts at basal conditions and after OXPHOS induction by galactose adaptation. We used cells with a stable expression of a pH-sensitive fluorescent mitochondrial reporter and applied state-of-the-art imaging techniques and image analysis. Our data showed a significant increase in acidic mitochondria after galactose adaptation. Using a machine-learning approach we also demonstrated increased mitochondrial fragmentation by OXPHOS induction. Furthermore, super-resolution microscopy of live cells enabled capturing of mitochondrial fragments within lysosomes as well as dynamic transfer of mitochondrial contents to lysosomes. Applying correlative light and electron microscopy we revealed the ultrastructure of the acidic mitochondria confirming their proximity to the mitochondrial network, ER and lysosomes. Finally, exploiting siRNA knockdown strategy combined with flux perturbation with lysosomal inhibitors, we demonstrated the importance of both canonical as well as non-canonical autophagy mediators in lysosomal degradation of mitochondria after OXPHOS induction. Taken together, our high-resolution imaging approaches applied on H9c2 cells provide novel insights on mitophagy during physiologically relevant conditions. The implication of redundant underlying mechanisms highlights the fundamental importance of mitophagy

Norwegian parents avoid placing infants in prone sleeping positions but frequently share beds in hazardous ways

Aim Campaigns to prevent prone sleeping and other modifiable risk factors have greatly reduced the incidence of sudden infant death syndrome in Norway. Sleep-related infant deaths still occur sporadically and may be preventable. We studied infants’ sleeping environments and whether parents followed safe sleep recommendations. Methods Parents with infants up to 12 months of age were invited to complete an online questionnaire from May to December 2018. It was publicised by health centres and on websites and social media. Results We received 4886 responses and 4150 met the age criteria and were included. Just under two-thirds (62.7%) reported routine bed-sharing, and this practice was associated with increased nocturnal breastfeeding, single parents and having more than one child. A small number of infants under six months were occasionally placed prone when they were laid down to sleep (2.1%) and 29.7% were placed on their side. Nearly three-quarters (72.6%) of the 2330 parents with infants under six months of age reported previous high-risk behaviour, such as sleeping together on a sofa or bed-sharing after smoking or drinking. Conclusion Norwegian parents rarely used prone sleeping positions for infants. However, bed-sharing was common, including high-risk scenarios such as smoking, alcohol use and sofas

Inflammation and reduced endothelial function in the course of severe acute heart failure

Systemic inflammation and elevated circulating levels of the endogenous nitric oxide inhibitor asymmetrical dimethylarginine (ADMA) have been associated with increased risk in cardiogenic shock (CS). In this prospective study, we assessed, over 4 consecutive days, the changes and possible associations between vascular function, markers of inflammation, and circulating ADMA levels in patients with CS (n = 12) and postcardiotomy heart failure (n = 12, PC-HF). Vasodilator function was measured as a reactive hyperemia index (RH-index) using a finger plethysmograph. Blood samples were analyzed for plasma ADMA, interleukine-6, interleukine-8, intracellular adhesion molecule-1, and vascular adhesion molecule-1. Baseline RH-index was significantly attenuated compared with healthy controls (2.28) for both CS and PC-HF (1.35 and 1.45, respectively, P = 0.001). Although vasodilator function improved in PC-HF patients, it remained attenuated in CS. Inflammatory markers were markedly elevated followed by a significant fall during the observation period in both groups. ADMA levels increased significantly during the observation period for PC-HF, whereas no pattern of change was observed for CS. No association was found between the longitudinal changes in RH-index, markers of inflammation, or ADMA in CS. However, an improved RH-index was associated with decreasing inflammatory markers in PC-HF. ADMA correlated to arterial lactate levels and the degree of organ dysfunction in CS. In conclusion, CS and PC-HF were characterized by a marked inflammatory activation accompanied by an attenuated vasodilator function. ADMA was related to organ dysfunction and degree of hypoperfusion during CS but showed no correlations to inflammation or hampered vasodilator function. The pathogenic significance of these responses needs clarificatio

Novel biomolecules of ageing, sex differences and potential underlying mechanisms of telomere shortening in coronary artery disease

Telomere length (TL), growth differentiate factor (GDF)11, insulin growth factor (IGF)1, sirtuin (SIRT)1 and inflammatory processes have been related to ageing and age-related diseases, like coronary artery disease (CAD). We aimed to investigate the associations between leukocyte TLs (LTLs), chronological age, sex and comorbidities in CAD patients. Any covariations between LTL, GDF11, IGF1, SIRT-1 and pro-inflammatory cytokines were further assessed. Methods In 300 patients with stable CAD (age 36–81 years, 20% females), DNA and RNA were isolated from whole blood for PCR analysis and relative quantification of LTLs and gene-expression of GDF11, IGF1,SIRT1, IL-12, IL-18 and IFNƴ, respectively. Serum was prepared for the analyses of circulating IL-18, IL-12, IL-6 and TNFα. Results Patients with previous myocardial infarction (MI) presented with 20% shorter LTLs vs. patients without (p = 0.019) indicating LTLs to be of importance for CAD severity. The observation however, was only observed in men (p = 0.009, n = 115), in which the upper LTL quartile associated with 64% lower frequency of previous MI compared to quartile 1–3 (p = 0.005, adjusted). LTLs were not differently distributed according to sex or comorbidities such as hypertension, diabetes type 2 and metabolic syndrome. LTLs and GDF11 were inversely correlated to age (r = −0.17; p = 0.007 and r = −0.16; p = 0.010, respectively), however, separated in gender, LTL only in women (r = −0.37) and GDF11 only in men (r = −0.19) (p = 0.006, both). GDF11 and SIRT1 were strongly inter-correlated (r = 0.56, p ≤ 0.001), suggesting common upstream regulators. LTLs were moderately correlated to GDF11 and SIRT1 in overweight women (BMI ≥ 25 kg/m2) (r = 0.41; p = 0.027 and 0.43; p = 0.020, respectively), which may reflect common life-style influences on LTLs and these markers. In all women, we observed further that the highest LTL quartile associated with higher GDF11 and SIRT expression and lower circulating levels of IL-12, IL-18 and TNFα, as compared to quartile 1, which may indicate lifestyle influences on female LTLs. In men, the highest LTL quartile associated with lower IFNƴ expression and lower circulating TNFα. Overall, the results indicate an association between chronic low-grade inflammation and LTLs. Conclusions Shorter LTLs in CAD patients with previously suffered MI may indicate telomere attrition as part of its pathophysiology in men. The inverse association between LTLs and age exclusively in women underpins the previously reported decline in attrition rate in men with increasing age. As elevated GDF11 and SIRT1 along with attenuated pro-inflammatory cytokines seem to positively affect LTL in women, we hypothesize a potential sex-dimorphism in LTL regulation, which may implicate sex- adjusted health-preventive therapies

Experiences of Norwegian Mothers Attending an Online Course of Therapeutic Writing Following the Unexpected Death of a Child

The unexpected death of a child is one of the most challenging losses as it fractures survivors’ sense of parenthood and other layers of identity. Given that not all the bereaved parents who have need for support respond well to available treatments and that many have little access to further intervention or follow-up over time, online interventions featuring therapeutic writing and peer support have strong potential. In this article we explore how a group of bereaved mothers experienced the process of participating in an online course in therapeutic writing for the integration of grief. Our research questions were: How do parents who have lost a child experience being part of an online course in therapeutic writing? What are the perceived benefits and challenges of writing in processing their grief? We followed an existential phenomenological approach and analyzed fieldwork notes (n = 13), qualitative data from the application and assessment surveys (n = 35; n = 21), excerpts from the journals of some participants (n = 3), and email correspondence with some participants (n = 5). We categorized the results in three meaning units: (1) where does my story begin? The “both and” of their silent chaos; (2) standing on the middle line: a pregnancy that does not end; (3) closures and openings: “careful optimism” and the need for community support. Participants experienced writing as an opportunity for self-exploration regarding their identities and their emotional world, as well as a means to develop and strengthen a bond with their children. They also experienced a sense of belonging, validation, and acceptance in the online group in a way that helped them make sense of their suffering. Online writing courses could be of benefit for bereaved parents who are grieving the unexpected death of a child, but do not replace other interventions such as psychotherapy. In addition to trauma and attachment informed models of grief, identity informed models with a developmental focus might enhance the impact of both low-threshold community interventions and more intensive clinical ones. Further studies and theoretical development in the area are needed, addressing dialogical notions such as the multivoicedness of the self

TERT and TET2 Genetic Variants Affect Leukocyte Telomere Length and Clinical Outcome in Coronary Artery Disease Patients—A Possible Link to Clonal Hematopoiesis

Inherited and acquired mutations in hematopoietic stem cells can cause clonal expansion with increased risk of cardiovascular disease (CVD), a condition known for the clonal hematopoiesis of indeterminate potential (CHIP). Inherited genetic variants in two CHIP-associated genome loci, the telomerase gene telomerase enzyme reverse transcriptase (TERT) (rs7705526) and the epigenetic regulator ten–eleven translocation 2 (TET2) (rs2454206), were investigated in 1001 patients with stable coronary artery disease (CAD) (mean age 62 years, 22% women), with regards to cardiovascular outcome, comorbidities, and leukocyte telomere length. Over 2 years, mutated TERT increased the risk two-fold for major clinical events (MACEs) in all patients (p = 0.004), acute myocardial infarction (AMI) in male patients (p = 0.011), and stroke in female patients (p < 0.001). Mutated TET2 correlated with type 2 diabetes (p < 0.001), the metabolic syndrome (p = 0.002), as well as fasting glucose, HbA1c, and shorter telomeres (p = 0.032, p = 0.003, and p = 0.016, respectively). In conclusion, our results from stable CAD patients highlight TERTs’ role in CVD, and underline TET2s’ role in the epigenetic regulation of lifestyle-related diseases

Biomarkers of ageing and cardiac remodeling are associated with atrial fibrillation

Objectives. Ageing is one of the strongest risk factors for atrial fibrillation (AF), and additional risk factors are also closely related to ageing. Remodeling is part of the pathophysiology of AF, and a possible common denominator of ageing and other AF risk factors. The aim of this study was to investigate any association between the presence of AF and the ageing biomarkers, leukocyte telomere length (LTL) and sirtuin-1 (SIRT-1), and the cardiac remodeling biomarkers Galectin-3 and sST2 in elderly myocardial infarction (MI) patients. Design. Patients were included after admission for MI. Diagnosis of AF was retrieved from medical records and classified as either history of AF before MI or new onset from admission to study inclusion. SIRT-1, sST2 and Galectin-3 were analyzed by ELISAs and LTL by qPCR. Results. In total, 299 patients were included, median age 75 years, 70.2% male. A history of AF was recorded in 38 patients and 30 patients experienced new onset AF. Higher levels of SIRT-1 were associated with lower risk of having a history of AF (OR = 0.46 (95% CI 0.26, 0.81), p = 0.007), whereas higher sST2 levels were associated with higher risk of AF (OR = 4.13 (95% CI 1.69, 10.13), p = 0.002). Results remained significant after adjustment for other AF risk factors. No significant associations with AF were found for Galectin-3 or LTL. None of the biomarkers associated with new onset AF. Conclusion. In elderly patients with MI, higher ST2 and lower SIRT-2 levels were associated with higher prevalence of AF, possibly reflecting both ageing and the remodeling phenomena in AF