Is rumination after bereavement linked with loss avoidance? : Evidence from eye-tracking

Funding: This research was funded by a Zon-MW TOP Grant of the Dutch Society for Scientific Research (NWO) under Grant number 91208009. Website: www.zonmw.nl. The funders had no role in the study design, data collection and analysis, decision to publish or preparation of the manuscript.Peer reviewedPublisher PD

The effectiveness of Grief-Help, a cognitive behavioural treatment for prolonged grief in children: study protocol for a randomised controlled trial

BACKGROUND: There is growing recognition of a syndrome of disturbed grief referred to as prolonged grief disorder (PGD). PGD is mostly studied in adults, but clinically significant PGD symptoms have also been observed in children and adolescents. Yet, to date no effective treatment for childhood PGD exists. The aims of this study are: (1) to investigate the effectiveness of Grief-Help, a nine-session cognitive-behavioural treatment for childhood PGD, combined with five sessions of parental counselling, immediately after the treatment and at three, six and twelve months follow-up; (2) to examine tentative mediators of the effects of Grief-Help, (i.e., maladaptive cognitions and behaviours and positive parenting), and (3) to determine whether demographic variables, child personality, as well as symptoms of PGD, anxiety, and depression in parents moderate the treatment effectiveness. METHODS/DESIGN: We will conduct a Randomised Controlled Trial (RCT) in which 160 children and adolescents aged 8–18 years are randomly allocated to cognitive behavioural Grief-Help or to a supportive counselling intervention; both treatments are combined with five sessions of parental counselling. We will recruit participants from clinics for mental health in the Netherlands. The primary outcome measure will be the severity of Prolonged Grief Disorder symptoms according to the Inventory of Prolonged Grief for Children (IPG-C). Secondary outcomes will include PTSD, depression and parent-rated internalizing and externalizing problems. Mediators like positive parenting and maladaptive cognitions and behaviours will be identified. We will also examine possible moderators including demographic variables (e.g. time since loss, cause of death), psychopathology symptoms in parents (PGD, anxiety and depression) and child personality. Assessments will take place in both groups at baseline, after the treatment-phase and three, six and twelve months after the post-treatment assessment. DISCUSSION: We aim to contribute to the improvement of mental health care for children and adolescents suffering from loss. By comparing Grief-Help with supportive counselling, and by investigating mediators and moderators of its effectiveness we hope to provide new insights in the effects of interventions for bereaved children, and their mechanisms of change. TRIAL REGISTRATION: Netherlands Trial Register NTR385

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OBJECTIVES: Rumination is a risk factor after bereavement, predicting higher concurrent and prospective symptom levels of complicated grief and depression in mourners. Research has shown that rumination may consist of adaptive and maladaptive subtypes, but there has been a paucity of research in this topic in the bereavement area. Therefore, we aimed to clarify whether functional and dysfunctional forms of rumination can be distinguished after loss. DESIGN: Two-hundred and forty-two adults, who lost a first-degree family member on average 10 months previously, filled out questionnaires at three time points with 6 months between each time point. METHODS: Multiple regression analyses, controlled for loss-related variables, neuroticism, and baseline symptoms, were run to examine associations of subtypes of depressive rumination (brooding, reflection) and grief rumination (rumination about injustice, meaning, reactions, relationships and counterfactual thinking) with concurrent and prospective symptom levels of complicated grief and depression. RESULTS: Overall, grief rumination explained more variance in symptom levels than depressive rumination. Other major findings were that grief rumination about injustice predicted higher concurrent and prospective symptom levels of complicated grief and higher prospective symptom levels of depression. In contrast, grief rumination about emotional reactions was related to prospective reductions in symptoms of complicated grief. Reflection was also associated with prospective reductions of complicated grief and depressive symptom levels. CONCLUSIONS: Results indicate that adaptive and maladaptive forms of ruminative thinking can be distinguished in bereaved individuals. Therapeutic interventions for complicated grief could potentially be improved by including techniques aimed at reducing maladaptive rumination and increasing adaptive rumination. PRACTITIONER POINTS: Clinical implications Adaptive and maladaptive components of rumination after loss can be distinguished. They are differentially associated with concurrent and prospective symptom levels of complicated grief and depression in mourners. Adaptive rumination after bereavement is characterized by repetitive, self-focused thinking aimed at understanding one's depressive and loss-related emotional reactions. Maladaptive rumination is characterized by repetitive, self-focused thinking about injustice to the self and making passive comparisons between the current situation (in which one has experienced a loss) and unrealized alternatives. Psychological interventions for complicated grief may be improved by adding therapeutic techniques aimed at reducing maladaptive rumination and increasing adaptive rumination. Cautions and limitations This investigation relied exclusively on self-report measures. Conjugally bereaved women were overrepresented in the current sample. Complicated grief and depression levels in the current sample ranged from non-clinical to clinical. Effects may be more pronounced in a clinical sample

Організація самостійної роботи студентів ВНЗів із вивчення лексичного матеріалу

Статтю присвячено проблемі підвищення продуктивності вивчення лексичного матеріалу студентами немовних вищих навчальних закладів.The article is devoted to the problem of rising productivity of learning new lexical material by students of non-linguistic high educational establishments

Novel sulphamoylated 2‑methoxy estradiol derivatives inhibit breast cancer migration by disrupting microtubule turnover and organization

BACKGROUND : The estrogen metabolite 2-methoxyestradiol (2ME2) and a number of synthesised derivatives have been shown to bind to microtubules thereby arresting cancer cells in mitosis which leads to apoptosis. In interphase cells, microtubules play an important role in the delivery of proteins to subcellular locations including the focal adhesions. In fact, focal adhesion dynamics and cell migration are in part regulated by microtubules. We hypothesised that novel 2ME2 derivatives can alter cell migration by influencing microtubule dynamics in interphase cells. In this report we describe 2ME2 derivatives that display anti-migratory capabilities in a metastatic breast cancer cell line through their effects on the microtubule network resulting in altered focal adhesion signalling and RhoA activity. METHODS : Cell migration was assayed using wound healing assays. To eliminate mitosis blockage and cell rounding as a confounding factor cell migration was also assessed in interphase blocked cells. Fluorescence confocal microscopy was used to visualise microtubule dynamics and actin cytoskeleton organisation while western blot analysis was performed to analyse focal adhesion signalling and RhoA activation. RESULTS : 2ME2 derivatives, ESE-one and ESE-15-one, inhibited cell migration in cycling cells as expected but equally diminished migration in cells blocked in interphase. While no significant effects were observed on the actin cytoskeleton, focal adhesion kinase activity was increased while RhoA GTPase activity was inhibited after exposure to either compound. Microtubule stability was increased as evidenced by the increased length and number of detyrosinated microtubules while at the same time clear disorganisation of the normal radial microtubule organisation was observed including multiple foci. CONCLUSIONS : ESE-15-one and ESE-one are potent migration inhibitors of metastatic breast cancer cells. This ability is coupled to alterations in focal adhesion signalling but more importantly is associated with severe disorganisation of microtubule dynamics and polarity. Therefore, these compounds may offer potential as anti-metastatic therapies.The National Research Foundation (NRF) of South Africa, the Cancer Association of South Africa (CANSA), the Medical Research Council (MRC) of South Africa, the Struwig Germishuysen Trust and the School of Medicine Research Committee of the University of Pretoria (RESCOM).http://www.cancerci.comgl2020Physiolog

Lowered expression of tumor suppressor candidate MYO1C stimulates cell proliferation, suppresses cell adhesion and activates AKT

Myosin-1C (MYO1C) is a tumor suppressor candidate located in a region of recurrent losses distal to TP53. Myo1c can tightly and specifically bind to PIP2, the substrate of Phosphoinositide 3-kinase (PI3K), and to Rictor, suggesting a role for MYO1C in the PI3K pathway. This study was designed to examine MYO1C expression status in a panel of wellstratified endometrial carcinomas as well as to assess the biological significance of MYO1C as a tumor suppressor in vitro. We found a significant correlation between the tumor stage and lowered expression of MYO1C in endometrial carcinoma samples. In cell transfection experiments, we found a negative correlation between MYO1C expression and cell proliferation, and MYO1C silencing resulted in diminished cell migration and adhesion. Cells expressing excess of MYO1C had low basal level of phosphorylated protein kinase B (PKB, a.k.a. AKT) and cells with knocked down MYO1C expression showed a quicker phosphorylated AKT (pAKT) response in reaction to serum stimulation. Taken together the present study gives further evidence for tumor suppressor activity of MYO1C and suggests MYO1C mediates its tumor suppressor function through inhibition of PI3K pathway and its involvement in loss of contact inhibition.Royal Physiographic Society in Lund (Nilsson-Ehle Foundation) with grant numbers 30928, 32705 and 36388: KV. Wilhelm and Martina Lundgren Foundation: KV, AB. Assar Gabrielsson Research Foundation for Clinical Cancer Research with grant numbers FB11-15, FB12-26, FB13-05, FB14-46 and FB15-45: KV. Sahlgrenska University Hospital Foundation with grant number 8181: KV. The Knowledge Foundation with grant number HOÈ G12, 20120311: AB.http://www.plosone.orgam2016Physiolog