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We highly welcome and appreciate the paper of Dieudonné, 2020 ( https//doi.org/10.1186/s12940-020-00602-0 ) on the important but frequently neglected topic of hypersensitivity towards electromagnetic fields (EHS). We agree with the author that the electromagnetic hypothesis (that EHS is caused by exposure to electromagnetic fields) appears scientifically largely unfounded and that other theoretical approaches focussing on psychological processes are more plausible and promising. In the view of the author, two such approaches exist, namely a "cognitive hypothesis" (derived from the comprehensive model by Van den Bergh et al., 2017) and an "attributive hypothesis" as suggested by the author. In this commentary, we want to argue (a) that the distinction between the cognitive and the attributive hypothesis is inaccurate at the conceptual level; (b) that the distinction is also misleading at the mechanistic level, due to an incorrect interpretation of the evidence related to the cognitive hypothesis; and (c) that, by using the term "cognitive hypothesis", the existing comprehensive model is inappropriately narrowed down without fully appreciating its explanatory power for the phenomena subsumed under both the cognitive and attributive hypothesis. Therefore, the original term "comprehensive model" should be used rather than the label "cognitive hypothesis".Mitochondria are important cellular organelles involved in many different functions, from energy generation and fatty acid oxidation to cell death regulation and immune responses. Accumulating evidence indicates that mitochondrial stress acts as a key trigger of innate immune responses. Critically, the dysfunctional mitochondria can be selectively eliminated by mitophagy. The elimination of dysfunctional mitochondria may function as an effective way employed by mitophagy to keep the immune system in check. In addition, mitophagy can be utilized by pathogens for immune evasion. In this review, we summarize how mitochondrial stress triggers innate immune responses and the roles of mitophagy in innate immunity and in infection, as well as the molecular mechanisms of mitophagy. Video Abstract.In this editorial we discuss the new 2020 World Health Organization guidelines on physical activity and sedentary behaviour and a series of related papers that are published simultaneously in IJBNPA. The new guidelines reaffirm that physical activity is a 'best buy' for public health and should be used to support governments to increase investment in policy and research to promote and ensure physical activity opportunities are available for everyone. New recommendations on sedentary behaviour and inclusion of specific guidelines for people living with disability and/or chronic disease and pregnant and postpartum women are major developments since 2010. We discuss research priorities, as well as policy implementation and the contribution to the sustainable development agenda. The new guidelines can catalyse the paradigm shifts needed to enable equitable opportunities to be physically active for everyone, everywhere, every day.

Thyroid autoimmunity (TAI) - the presence of anti-thyroid peroxidase and/or anti-thyroglobulin antibodies - affects 8-14% of reproductively-aged women. It is hotly debated whether TAI adversely affects IVF/ICSI outcomes. This systematic review and meta-analysis evaluated the relationship between thyroid autoimmunity (TAI) and IVF/ICSI outcomes, both overall and amongst euthyroid women of known age using strict criteria for grouping pregnancy outcomes.

The review was registered with PROSPERO CRD42019120947. Searches were undertaken in MEDLINE, EMBASE, Web of Science and Cochrane Database from Inception-March 2020. Primary outcomes were clinical pregnancy rate, clinical miscarriage rate, biochemical pregnancy loss, livebirth rate per-cycle and live birth rate per clinical pregnancy (CP).

14 studies were included in the meta-analysis. Compared with women who tested negative for thyroid autoantibodies (TAI-), there was no significant difference in clinical pregnancy rate overall (OR 0.86; 95%CI [0.70, 1.05]thyroid women alone, or in euthyroid women and women with subclinical hypothyroidism.

The findings of the present study suggest that thyroid autoimmunity has no effect on pregnancy outcomes in euthyroid women alone, or in euthyroid women and women with subclinical hypothyroidism.

The inflammatory response after aneurysmal subarachnoid haemorrhage (aSAH) has been associated with early brain injury, delayed cerebral ischaemia, poor functional outcome, and case fatality. In experimental SAH studies, complement C5 antibodies administered shortly after SAH reduced brain injury with approximately 40%. Complement component C5 may be a new therapeutic target to reduce brain injury and hereby improve the outcome after aSAH. We aim to investigate the pharmacodynamic efficacy and safety of eculizumab (complement C5 antibody) in patients with aSAH.

A randomised, controlled, open-label, phase II clinical trial with blinded outcome assessment. Eculizumab (1200 mg) is administered intravenously < 12 h, on day 3 and on day 7 after ictus. Patients in the intervention group receive prophylactic antibiotics for 4 weeks, and those with a central line or an external ventricular shunt and a positive fungal or yeast culture also receive prophylactic antifungal therapy for 4 weeks. read more The primary outcome is C5a concentration in the cerebrospinal fluid (CSF) on day 3 after ictus. Secondary outcomes include the occurrence of adverse events, inflammatory parameters in the blood and CSF, cerebral infarction on magnetic resonance imaging, and clinical and cognitive outcomes. We aim to evaluate 26 patients with CSF assessments, 13 in the intervention group and 13 in the comparator group. To compensate for early case fatality and inability to obtain CSF, we will include 20 patients per group.

The CLASH trial is the first trial to investigate the pharmacodynamic efficacy and safety of eculizumab in the early phase after aSAH.

Netherlands Trial Register NTR6752 . Registered on 27 October 2017 European Clinical Trials Database (EudraCT) 2017-004307-51.

Netherlands Trial Register NTR6752 . Registered on 27 October 2017 European Clinical Trials Database (EudraCT) 2017-004307-51.

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