Online prevention of disordered eating in at-risk young-adult women: A two-country pragmatic randomized controlled trial

This article has been published in a revised form in Psychological Medicine. This version is free to view and download for private research and study only. Not for re-distribution, re-sale or use in derivative works. © Cambridge University Press 2017. This author accepted manuscript is made available following 6 month embargo from date of publication (Dec 2017) in accordance with the publisher’s copyright policyDisordered eating (DE) is a widespread, serious problem. Efficacious prevention programs that can be delivered at-scale are needed. A pragmatic randomized controlled trial of two online programs was conducted. Participants were young-adult women from Australia and New Zealand seeking to improve their body image. Media Smart-Targeted (MS-T) and Student Bodies (SB) were both 9-module interventions released weekly, whilst control participants received positive body image information. Primary [Eating Disorder Examination–Questionnaire (EDE-Q) Global], secondary (DE risk factors) and tertiary (DE) outcome measures were completed at baseline, post-program, 6- and 12-month follow-up. Baseline was completed by 608 women (M age = 20.71 years); 33 were excluded leaving 575 randomized to: MS-T (N = 191); SB (N = 190) or control (N = 194). Only 66% of those randomized to MS-T or SB accessed the intervention and were included in analyses with controls; 78% of this sample completed measures subsequent to baseline. Primary intent-to-treat (ITT) analyses revealed no differences between groups, while measure completer analyses found MS-T had significantly lower EDE-Q Global than controls at 12-month follow-up. Secondary ITT analyses found MS-T participants reported significantly higher quality of life–mental relative to both SB and controls (6-month follow-up), while MS-T and controls had lower clinical impairment relative to SB (post-program). Amongst measure completers, MS-T scored significantly lower than controls and SB on 5 variables. Of those with baseline DE, MS-T participants were significantly less likely than controls to have DE at 12-month follow-up. Given both programs were not therapist-moderated, MS-T has potential to achieve reductions in DE risk at low implementation costs

Skeletal Muscle - one year on

Background: Skeletal muscle differentiation is required for the regeneration of myofibers after injury. The differentiation capacity of satellite cells is impaired in settings of old age, which is at least one factor in the onset of sarcopenia – the age-related loss of skeletal muscle mass and major cause of frailty. One important cause for impaired regeneration is increased TGF-beta accompanied by reduced Notch signaling. Pro-inflammatory cytokines are also upregulated in ageing which led us hypothesize their potential contribution to impaired regeneration in sarcopenia. Thus, we have further analysed the muscle differentiation-inhibition pathway by pro-inflammatory cytokines in human skeletal muscle cells Methods: We studied the modulation of human skeletal muscle cell (HuSKMCs) differentiation by pro-inflammatory cytokines IL-1alpha and TNF-alpha. Grade of differentiation was determined by either imaging (fusion index) or creatine kinase (CK) activity, a marker of muscle differentiation. Secretion of TGF-beta proteins during differentiation was assessed by using a TGF-beta responsive reporter gene assay and further identified by means of pharmacological and genetic inhibitors. In addition, signaling events were monitored both in HuSKMC cultures as well as samples from a rat sarcopenia study by Western Blots and RT-PCR. Results: The pro-inflammatory cytokines IL-1α and TNF-α block differentiation of human myoblasts into myotubes. This anti-differentiation effect requires the activation of TAK-1. Using pharmacological and genetic inhibitors, the TAK-1 pathway could be traced to p38 and NFkappaB. Surprisingly, the anti-differentiation effect of the cytokines required the transcriptional upregulation of Activin A, which in turn acted through its established signaling pathway – ActRII/ALK/SMAD. Inhibition of Activin A signaling is able to rescue human myoblasts treated with IL-1alpha or TNF-α, resulting in normal differentiation into myotubes. Studies in aged rats as a model of sarcopenia confirmed that this pro-inflammatory cytokine pathway identified is activated during aging. Conclusions: This study demonstrates an unexpected connection between cytokine and Activin signaling, demonstrating a new mechanism by which cytokines affect skeletal muscle, establishing the physiologic relevance of this pathway in sarcopenia

FTO listens rolle

Formålet for denne opgave er, at komme nærmere USA’s Foreign Terrorist Organization liste (FTO liste). Vi undersøger listens sanktioner; hvordan de er tilsigtet samt diskuterer hvilke fordele og ulemper der taler for sanktionerne. Fokus lægges på finansieringen af terrorisme, da sanktionerne mest rammer dette område. Dog berøres andet terrorbekæmpelse. Ud fra dette konkluderer vi at; terrorisme opererer ulovligt for at skaffe finansiering, hvilket nedsætter FTO listens effektivitet. Desuden er terrorister utrolig tilpassende. Dog er listen juridisk anerkendt af stater og bringer klarhed over området, samt den bringer utvivlsomt resultater; listens sanktioner har bremset en del terrorfinansiering – selvom det uden tvivl er delvise resultater, er der ingen tvivl om at listen spiller en vis påkrævet rolle i terrorbekæmpelsen

The distribution, impact and potential management of the introdued vine Passiflora mollissima (Passifloraceae) in Hawai'i

Reports were scanned in black and white at a resolution of 600 dots per inch and were converted to text using Adobe Paper Capture Plug-in.Passiflora mollissima, a weedy vine introduced to Hawai'i, infests significant portions of two of the major islands, Hawai'i and Kaua'i. It grows between 600 and 2200 m elevation in areas where the rainfall does not exceed 5100 mm. The vine is distributed continuously over a total of 190 km² and in more widely scattered populations over an additional 330 km². Man has been the principle agent of introduction for this species. However, intermediate-distance dispersal may be affected by introduced gallincaeous birds and cattle. Locally feral pigs are the major dispersal agent. Passiflora mollissima inhabits many of the major upland vegetation types in Hawaii but is most successful in mesic Acacia koa - Metrosideros polymorpha forests. Although over much of its current range its foliage cover is less than 25%, in some areas it is so dense that it smothers large tracts of native forest. Potential impacts of the infestation on depleted and endangered endemic organisms are also discussed. It is concluded that P. mollissima has become too widespread for successful mechanical or chemical control except in are as of recent local introduction. Prospects for biological control of this species are discussed in the context of current research efforts and practical problems related to a commercially grown congener.U.S. Fish and Wildlife Service; Cooperative National Parks Reseach Studies Unit, Department of Botany, University of Hawai’i; Institute of Pacific Islands Forestry, U.S. Forest Service; Hawaii Volcanoes National Park, Resources Management Division; Hawaii Office of the Nature Conservanc

FGF22 signaling regulates synapse formation during post‐injury remodeling of the spinal cord

The remodeling of axonal circuits after injury requires the formation of new synaptic contacts to enable functional recovery. Which molecular signals initiate such axonal and synaptic reorganisation in the adult central nervous system is currently unknown. Here, we identify FGF22 as a key regulator of circuit remodeling in the injured spinal cord. We show that FGF22 is produced by spinal relay neurons, while its main receptors FGFR1 and FGFR2 are expressed by cortical projection neurons. FGF22 deficiency or the targeted deletion of FGFR1 and FGFR2 in the hindlimb motor cortex limits the formation of new synapses between corticospinal collaterals and relay neurons, delays their molecular maturation, and impedes functional recovery in a mouse model of spinal cord injury. These results establish FGF22 as a synaptogenic mediator in the adult nervous system and a crucial regulator of synapse formation and maturation during post‐injury remodeling in the spinal cord.SynopsisFollowing spinal cord injury, transected projections form detour circuits that circumvent the lesion and contribute to functional recovery. The formation of new synaptic contacts is a crucial step of the process, but its molecular regulation is currently not understood. Members of the FGF family can promote synapse formation during nervous system development, suggesting that they might have a similar function in the injured adult CNS. Here, we show that:FGF22 and FGF22 receptors are expressed in the adult nervous system.FGF22 deficiency or deletion of FGF22 receptors restricts the formation and maturation of new synapses in the injured spinal cord.Genetic disruption of FGF22 signaling impedes spontaneous functional recovery following spinal cord injury.FGF22 is a synaptogenic mediator in the adult nervous system and promotes synaptic plasticity and circuit remodeling in a mouse model of spinal cord injury.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/111756/1/embj201490578-sup-0001-Suppl_Info.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/111756/2/embj201490578.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/111756/3/embj201490578.reviewer_comments.pd

Formation of somatosensory detour circuits mediates functional recovery following dorsal column injury

Anatomically incomplete spinal cord injuries can be followed by functional recovery mediated, in part, by the formation of intraspinal detour circuits. Here, we show that adult mice recover tactile and proprioceptive function following a unilateral dorsal column lesion. We therefore investigated the basis of this recovery and focused on the plasticity of the dorsal column-medial lemniscus pathway. We show that ascending dorsal root ganglion (DRG) axons branch in the spinal grey matter and substantially increase the number of these collaterals following injury. These sensory fibers exhibit synapsin-positive varicosities, indicating their integration into spinal networks. Using a monosynaptic circuit tracing with rabies viruses injected into the cuneate nucleus, we show the presence of spinal cord neurons that provide a detour pathway to the original target area of DRG axons. Notably the number of contacts between DRG collaterals and those spinal neurons increases by more than 300% after injury. We then characterized these interneurons and showed that the lesion triggers a remodeling of the connectivity pattern. Finally, using re-lesion experiments after initial remodeling of connections, we show that these detour circuits are responsible for the recovery of tactile and proprioceptive function. Taken together our study reveals that detour circuits represent a common blueprint for axonal rewiring after injury