Establishing sexual assault care centres in Belgium : health professionals' role in the patient-centred care for victims of sexual violence

Background: Having ratified the Convention of Istanbul, the Belgian federal government commits itself to the foundation of Sexual Assault Care Centres (SACC). In the light of researching the feasibility of these centres, this study aimed to evaluate the care for victims of sexual violence (SV) in Belgian hospitals anno 2016 as well as to formulate recommendations for the intended model. Methods: Between April and October 2016, a questionnaire was distributed to 159 key health professionals active in 17 different hospitals attached to an AIDS Referral Centre. The survey covered four parts, i.e. the health professionals' profile, their knowledge, attitude and practices, an assessment of the hospital's policy and the caregivers' opinion on the care for victims of SV and on the intended SACCs. Subsequently, a descriptive analysis using IBM SPSS Statistics 23' was performed. Results: A total of 60 key health professionals representing 15 different hospitals completed the questionnaire resulting in a response rate of 38%. The results showed a lack of knowledge and practical experience of caregivers' regarding the care for SV victims. Approximately 30% of responders face personal or professional difficulties upon provision of care to victims of SV. Participants evaluate the current care as good, despite the limited psychosocial support, follow-up, insight for the needs of vulnerable groups and support for family, relatives and health professionals. Yet, the majority of health professionals appraise the SACCs as the best approach for both victims and caregivers. Conclusions: By introducing a SACC, the Belgian federal government aims to provide holistic and patient-centred care for victims of SV. Essential in patient-centred health care is an extensive and continuous education, training and supervision of health professionals concerning the care for victims, support for family, relatives and caregivers. At the end and as a result of a participatory process with many professional experts as well as victims, a specific Belgian model, adjusted to the health care system anno 2016 was developed for piloting. The main challenges in establishing SACCs are situated at the institutional and policy level. Collaborating with other institutions and further research are herewith required

European achievements in soil remediation and brownfield redevelopment

With the aim of sharing best practices of soil restoration and management of contaminated sites among European countries and to raise awareness of the enormous efforts made to succeed in such difficult commitment, the experts of the EIONET Soil working group on contaminated sites and brownfields agreed to gather their country's interesting cases and successful stories of recovery of contaminated areas. This second edition of the monograph presents seventeen new cases from eight European countries and its Regions of how polluted sites and brownfields have been remediated like new methodologies of sustainable restoration of the subsoil, development of innovative technologies, and funding mechanisms etc. These stories have been compiled to present what national, regional or local governments are doing to improve the quality of the environment and the living conditions of their population. A second aim is the promotion of best practices among industry, consultancies and business operators.JRC.D.3-Land Resource

Loss of DPP6 in neurodegenerative dementia : a genetic player in the dysfunction of neuronal excitability

Emerging evidence suggested a converging mechanism in neurodegenerative brain diseases (NBD) involving early neuronal network dysfunctions and alterations in the homeostasis of neuronal firing as culprits of neurodegeneration. In this study, we used paired-end short-read and direct long-read whole genome sequencing to investigate an unresolved autosomal dominant dementia family significantly linked to 7q36. We identified and validated a chromosomal inversion of ca. 4Mb, segregating on the disease haplotype and disrupting the coding sequence of dipeptidyl-peptidase 6 gene (DPP6). DPP6 resequencing identified significantly more rare variants-nonsense, frame-shift, and missense-in early-onset Alzheimer's disease (EOAD, p value = 0.03, OR = 2.21 95% CI 1.05-4.82) and frontotemporal dementia (FTD, p = 0.006, OR = 2.59, 95% CI 1.28-5.49) patient cohorts. DPP6 is a type II transmembrane protein with a highly structured extracellular domain and is mainly expressed in brain, where it binds to the potassium channel K(v)4.2 enhancing its expression, regulating its gating properties and controlling the dendritic excitability of hippocampal neurons. Using in vitro modeling, we showed that the missense variants found in patients destabilize DPP6 and reduce its membrane expression (p < 0.001 and p < 0.0001) leading to a loss of protein. Reduced DPP6 and/or K(v)4.2 expression was also detected in brain tissue of missense variant carriers. Loss of DPP6 is known to cause neuronal hyperexcitability and behavioral alterations in Dpp6-KO mice. Taken together, the results of our genomic, genetic, expression and modeling analyses, provided direct evidence supporting the involvement of DPP6 loss in dementia. We propose that loss of function variants have a higher penetrance and disease impact, whereas the missense variants have a variable risk contribution to disease that can vary from high to low penetrance. Our findings of DPP6, as novel gene in dementia, strengthen the involvement of neuronal hyperexcitability and alteration in the homeostasis of neuronal firing as a disease mechanism to further investigate

Current care for victims of sexual violence and future sexual assault care centres in Belgium: The perspective of victims

Background: Sexual violence is a global health problem. After ratifying the Convention of Istanbul in 2016, this Belgian study was set up to map the perspective of victims of rape on the current sexual violence care provision in Belgium and to inquire on their need for more specialised and holistic care in future Sexual Assault Care Centres. Methods: Sixteen rape victims participated in this sub-study. A mixed-method design (questionnaire, in-depth interview or small focus group) was applied depending on the time elapsed between rape and participation. Descriptive Thematic Framework Analysis was performed in duo. Results: The participants thought it of utmost importance that every victim should receive all medical, psychological and forensic care without necessarily having to involve the police first. They stated that the current Belgian sexual violence care provision could be much more patient-centred, specifically the forensic examination and psychological care. Alongside medical and psychological consequences, victims emphasised the high personal financial and relational burden of sexual violence. The holistic care offered in Sexual Assault Care Centres was perceived to enhance the recovery process of victims of sexual violence. Their doors should be open to all victims and their relatives. They should not only provide acute care for the victim, but also improve victims' reintegration into society while reducing their personal costs significantly. Conclusion: All care for victims of sexual violence, especially forensic and psychological care, needs drastic improvement in Belgium. All participants agreed that having specialised, multidisciplinary and longitudinal care in a Sexual Assault Care Centre that would be open 24/7 for everyone, victims and their significant others, would be an improvement to the currently available care all over Belgium. Trial registration: This research was registered on April 1st 2016. Registration number B670201628242.SCOPUS: ar.jinfo:eu-repo/semantics/publishe

Loss ofTBK1is a frequent cause of frontotemporal dementia in a Belgian cohort

Objective: To assess the genetic contribution of TBK1, a gene implicated in amyotrophic lateral sclerosis (ALS), frontotemporal dementia (FTD), and FTD-ALS, in Belgian FTD and ALS patient cohorts containing a significant part of genetically unresolved patients. Methods: We sequenced TBK1 in a hospital-based cohort of 482 unrelated patients with FTD and FTD-ALS and 147 patients with ALS and an extended Belgian FTD-ALS family DR158. We followed up mutation carriers by segregation studies, transcript and protein expression analysis, and immunohistochemistry. Results: We identified 11 patients carrying a loss-of-function (LOF) mutation resulting in an overall mutation frequency of 1.7% (11/629), 1.1% in patients with FTD (5/460), 3.4% in patients with ALS (5/147), and 4.5% in patients with FTD-ALS (1/22). We found 1 LOF mutation, p.Glu643del, in 6 unrelated patients segregating with disease in family DR158. Of 2 mutation carriers, brain and spinal cord was characterized by TDP-43-positive pathology. The LOF mutations including the p.Glu643del mutation led to loss of transcript or protein in blood and brain. Conclusions: TBK1 LOF mutations are the third most frequent cause of clinical FTD in the Belgian clinically based patient cohort, after C9orf72 and GRN, and the second most common cause of clinical ALS after C9orf72. These findings reinforce that FTD and ALS belong to the same disease continuum

Loss of TBK1 is a frequent cause of frontotemporal dementia in a Belgian cohort

Objective:To assess the genetic contribution of TBK1, a gene implicated in amyotrophic lateral sclerosis (ALS), frontotemporal dementia (FTD), and FTD-ALS, in Belgian FTD and ALS patient cohorts containing a significant part of genetically unresolved patients.Methods:We sequenced TBK1 in a hospital-based cohort of 482 unrelated patients with FTD and FTD-ALS and 147 patients with ALS and an extended Belgian FTD-ALS family DR158. We followed up mutation carriers by segregation studies, transcript and protein expression analysis, and immunohistochemistry.Results:We identified 11 patients carrying a loss-of-function (LOF) mutation resulting in an overall mutation frequency of 1.7% (11/629), 1.1% in patients with FTD (5/460), 3.4% in patients with ALS (5/147), and 4.5% in patients with FTD-ALS (1/22). We found 1 LOF mutation, p.Glu643del, in 6 unrelated patients segregating with disease in family DR158. Of 2 mutation carriers, brain and spinal cord was characterized by TDP-43-positive pathology. The LOF mutations including the p.Glu643del mutation led to loss of transcript or protein in blood and brain.Conclusions:TBK1 LOF mutations are the third most frequent cause of clinical FTD in the Belgian clinically based patient cohort, after C9orf72 and GRN, and the second most common cause of clinical ALS after C9orf72. These findings reinforce that FTD and ALS belong to the same disease continuum

Loss of DPP6 in neurodegenerative dementia: a genetic player in the dysfunction of neuronal excitability.

Emerging evidence suggested a converging mechanism in neurodegenerative brain diseases (NBD) involving early neuronal network dysfunctions and alterations in the homeostasis of neuronal firing as culprits of neurodegeneration. In this study, we used paired-end short-read and direct long-read whole genome sequencing to investigate an unresolved autosomal dominant dementia family significantly linked to 7q36. We identified and validated a chromosomal inversion of ca. 4 Mb, segregating on the disease haplotype and disrupting the coding sequence of dipeptidyl-peptidase 6 gene (DPP6). DPP6 resequencing identified significantly more rare variants-nonsense, frameshift, and missense-in early-onset Alzheimer's disease (EOAD, p value = 0.03, OR = 2.21 95% CI 1.05-4.82) and frontotemporal dementia (FTD, p = 0.006, OR = 2.59, 95% CI 1.28-5.49) patient cohorts. DPP6 is a type II transmembrane protein with a highly structured extracellular domain and is mainly expressed in brain, where it binds to the potassium channel K4.2 enhancing its expression, regulating its gating properties and controlling the dendritic excitability of hippocampal neurons. Using in vitro modeling, we showed that the missense variants found in patients destabilize DPP6 and reduce its membrane expression (p < 0.001 and p < 0.0001) leading to a loss of protein. Reduced DPP6 and/or K4.2 expression was also detected in brain tissue of missense variant carriers. Loss of DPP6 is known to cause neuronal hyperexcitability and behavioral alterations in Dpp6-KO mice. Taken together, the results of our genomic, genetic, expression and modeling analyses, provided direct evidence supporting the involvement of DPP6 loss in dementia. We propose that loss of function variants have a higher penetrance and disease impact, whereas the missense variants have a variable risk contribution to disease that can vary from high to low penetrance. Our findings of DPP6, as novel gene in dementia, strengthen the involvement of neuronal hyperexcitability and alteration in the homeostasis of neuronal firing as a disease mechanism to further investigate