Employer Attitudes towards Peak Hour Avoidance

Peak Hour Avoidance is a relatively new Dutch mobility management measure. To reduce congestion frequent car drivers are given a financial reward for reducing the proportion of trips that they make during peak hours on a specific motorway section. Although previous studies show that employers are not eager to support mobility management measures, employers are nevertheless an important stakeholder. They can provide their employees with alternatives such as other travel times, work locations or travel modes and encourage their use. This paper investigates the attitudes of Dutch employers towards Peak Hour Avoidance. Exploring the factors that influence these attitudes may help to fully utilise employer support. The data from 103 employers were collected through a web questionnaire. A structural equation model on the employer support for Peak Hour Avoidance was estimated. The results demonstrate that the size of the organisation and sector only have an indirect effect on the support for Peak Hour Avoidance. Results reveal that most support for Peak Hour Avoidance can be expected from organisations who feel responsible for influencing the commuting behaviour of employees, that have human resource managers with a positive attitude towards Peak Hour Avoidance, with flexible working times and that have already implemented mobility management measures. The largest contribution to PHA that can be expected from employers is providing employees with flexible working times and encouraging employees to fully utilise this option as an alternative for driving in peak hours. This would not only be beneficial for PHA but for a wide range of mobility management initiatives as well

Bi-allelic Loss-of-Function CACNA1B Mutations in Progressive Epilepsy-Dyskinesia.

The occurrence of non-epileptic hyperkinetic movements in the context of developmental epileptic encephalopathies is an increasingly recognized phenomenon. Identification of causative mutations provides an important insight into common pathogenic mechanisms that cause both seizures and abnormal motor control. We report bi-allelic loss-of-function CACNA1B variants in six children from three unrelated families whose affected members present with a complex and progressive neurological syndrome. All affected individuals presented with epileptic encephalopathy, severe neurodevelopmental delay (often with regression), and a hyperkinetic movement disorder. Additional neurological features included postnatal microcephaly and hypotonia. Five children died in childhood or adolescence (mean age of death: 9 years), mainly as a result of secondary respiratory complications. CACNA1B encodes the pore-forming subunit of the pre-synaptic neuronal voltage-gated calcium channel Cav2.2/N-type, crucial for SNARE-mediated neurotransmission, particularly in the early postnatal period. Bi-allelic loss-of-function variants in CACNA1B are predicted to cause disruption of Ca2+ influx, leading to impaired synaptic neurotransmission. The resultant effect on neuronal function is likely to be important in the development of involuntary movements and epilepsy. Overall, our findings provide further evidence for the key role of Cav2.2 in normal human neurodevelopment.MAK is funded by an NIHR Research Professorship and receives funding from the Wellcome Trust, Great Ormond Street Children's Hospital Charity, and Rosetrees Trust. E.M. received funding from the Rosetrees Trust (CD-A53) and Great Ormond Street Hospital Children's Charity. K.G. received funding from Temple Street Foundation. A.M. is funded by Great Ormond Street Hospital, the National Institute for Health Research (NIHR), and Biomedical Research Centre. F.L.R. and D.G. are funded by Cambridge Biomedical Research Centre. K.C. and A.S.J. are funded by NIHR Bioresource for Rare Diseases. The DDD Study presents independent research commissioned by the Health Innovation Challenge Fund (grant number HICF-1009-003), a parallel funding partnership between the Wellcome Trust and the Department of Health, and the Wellcome Trust Sanger Institute (grant number WT098051). We acknowledge support from the UK Department of Health via the NIHR comprehensive Biomedical Research Centre award to Guy's and St. Thomas' National Health Service (NHS) Foundation Trust in partnership with King's College London. This research was also supported by the NIHR Great Ormond Street Hospital Biomedical Research Centre. J.H.C. is in receipt of an NIHR Senior Investigator Award. The research team acknowledges the support of the NIHR through the Comprehensive Clinical Research Network. The views expressed are those of the author(s) and not necessarily those of the NHS, the NIHR, Department of Health, or Wellcome Trust. E.R.M. acknowledges support from NIHR Cambridge Biomedical Research Centre, an NIHR Senior Investigator Award, and the University of Cambridge has received salary support in respect of E.R.M. from the NHS in the East of England through the Clinical Academic Reserve. I.E.S. is supported by the National Health and Medical Research Council of Australia (Program Grant and Practitioner Fellowship)

Pulmonary hypertension in heart failure with preserved ejection fraction: a plea for proper phenotyping and further research

Heart failure (HF) with preserved ejection fraction (HFpEF) is a common disease affecting the elderly in particular. Up to 80% of these patients develop pulmonary hypertension (PH), which is associated with worse symptoms and increased mortality.1 It is a matter of concern that drugs approved for pulmonary arterial hypertension (PAH) are sometimes used in such patients despite insufficient data for their safety and efficacy. On the other hand, the impact of PH and right ventricular (RV) dysfunction on morbidity and mortality in HFpEF call for proper attention both at the clinical and scientific level. Here we discuss the clinical problem, pathophysiology, diagnostic shortfalls, gaps in evidence, and future strategies for PH-HFpEF.SCOPUS: ar.jinfo:eu-repo/semantics/publishe