254 research outputs found
Physical Disability, Stigma, and Physical Activity in Children - A Replica Study
Introduction: Stereotypes can be reduced through positive descriptions. A stigma that able-bodied adults have towards children with physical disability can be reduced when the child is portrayed as being active. The study found out that a sporty active child, who uses a wheelchair, is perceived as more competent than the sporty active able-bodied child.
Objective: This study is a replica study to support the hypotheses and to examine the stereotypes of able-bodied adults towards children with and without (physical) disabilities.
Methods: This study presents two experimental replica studies using a 2 (physical activity) x 2 (sporty activities). The dependent variables were the perception of competencies and warmth according to Stereotype Content Model (SCM). Study 1 is an online experiment with 355 students of the Open University of Hagen. Study 2 surveys 1176 participants (from Munich and Graz) with a paper-pencil-questionnaire.
Results: The significant interaction effect was not supported by our studies.
The sporty able-bodied child was rated higher in competences than the sporty child, who use a wheelchair. Sporting activity only reduces the stigma towards children with a physical disability slightly.
Conclusion: The stigma towards children with physical disability can be reduced when the child is portrayed as being active, but the effect was not strong enough to chance the original classification by the SCM
Feasibility and cost description of highly intensive rehabilitation involving new technologies in patients with post-acute stroke-a trial of the Swiss RehabTech Initiative
BACKGROUND
There is a need to provide highly repetitive and intensive therapy programs for patients after stroke to improve sensorimotor impairment. The employment of technology-assisted training may facilitate access to individualized rehabilitation of high intensity. The purpose of this study was to evaluate the safety and acceptance of a high-intensity technology-assisted training for patients after stroke in the subacute or chronic phase and to establish its feasibility for a subsequent randomized controlled trial.
METHODS
A longitudinal, multi-center, single-group study was conducted in four rehabilitation clinics. Patients participated in a high-intensity 4-week technology-assisted trainings consisting of 3 to 5 training days per week and at least 5 training sessions per day with a duration of 45 min each. Feasibility was evaluated by examining recruitment, intervention-related outcomes (adherence, subjectively perceived effort and effectiveness, adverse events), patient-related outcomes, and efficiency gains. Secondary outcomes focused on all three domains of the International Classification of Functioning Disability and Health. Data were analyzed and presented in a descriptive manner.
RESULTS
In total, 14 patients after stroke were included. Participants exercised between 12 and 21 days and received between 28 and 82 (mean 46 ± 15) technology-assisted trainings during the study period, which corresponded to 2 to 7 daily interventions. Treatment was safe. No serious adverse events were reported. Minor adverse events were related to tiredness and exertion. From baseline to the end of the intervention, patients improved in several functional performance assessments of the upper and lower extremities. The efficiency gains of the trainings amounted to 10% to 58%, in particular for training of the whole body and for walking training in severely impaired patients.
CONCLUSIONS
Highly intensive technology-assisted training appears to be feasible for in- and outpatients in the subacute or chronic phase after stroke. Further clinical trials are warranted in order to define the most comprehensive approach to highly intensive technology-assisted training and to investigate its efficacy in patients with neurological disorders.
TRIAL REGISTRATION
ClinicalTrials.gov Identifier: NCT03641651 at August 31st 2018
Expression of interleukin-16 by tumor-associated macrophages/activated microglia in high-grade astrocytic brain tumors
Cryptotephras in the Lateglacial ICDP Dead Sea sediment record and their implications for chronology
Bub1 is activated by the protein kinase p90Rsk during Xenopus oocyte maturation
AbstractBackground: The kinetochore attachment (spindle assembly) checkpoint arrests cells in metaphase to prevent exit from mitosis until all the chromosomes are aligned properly at the metaphase plate. The checkpoint operates by preventing activation of the anaphase-promoting complex (APC), which triggers anaphase by degrading mitotic cyclins and other proteins. This checkpoint is active during normal mitosis and upon experimental disruption of the mitotic spindle. In yeast, the serine/threonine protein kinase Bub1 and the WD-repeat protein Bub3 are elements of a signal transduction cascade that regulates the kinetochore attachment checkpoint. In mammalian cells, activated MAPK is present on kinetochores during mitosis and activity is upregulated by the spindle assembly checkpoint. In vertebrate unfertilized eggs, a special form of meiotic metaphase arrest by cytostatic factor (CSF) is mediated by MAPK activation of the protein kinase p90Rsk, which leads to inhibition of the APC. However, it is not known whether CSF-dependent metaphase arrest caused by p90Rsk involves components of the spindle assembly checkpoint.Results: xBub1 is present in resting oocytes and its protein level increases slightly during oocyte maturation and early embryogenesis. In Xenopus oocytes, Bub1 is localized to kinetochores during both meiosis I and meiosis II, and the electrophoretic mobility of Bub1 upon SDS-PAGE decreases during meiosis I, reflecting phosphorylation and activation of the enzyme. The activation of Bub1 can be induced in interphase egg extracts by selective stimulation of the MAPK pathway by c-Mos, a MAPKKK. In oocytes treated with the MEK1 inhibitor U0126, the MAPK pathway does not become activated, and Bub1 remains in its low-activity, unshifted form. Injection of a constitutively active target of MAPK, the protein kinase p90Rsk, restores the activation of Bub1 in the presence of U0126. Moreover, purified p90Rsk phosphorylates Bub1 in vitro and increases its protein kinase activity.Conclusions: Bub1, an upstream component of the kinetochore attachment checkpoint, is activated during meiosis in Xenopus in a MAPK-dependent manner. Moreover, a single substrate of MAPK, p90Rsk, is sufficient to activate Bub1 in vitro and in vivo. These results indicate that in vertebrate eggs, kinetochore attachment/spindle assembly checkpoint proteins, including Bub1, are downstream of p90Rsk and may be effectors of APC inhibition and CSF-dependent metaphase arrest by p90Rsk
New insights into lake responses to rapid climate change : the Younger Dryas in Lake Goscia(z) over dot, central Poland
The sediment profile from Lake Goscia(z) over dot in central Poland comprises a continuous, seasonally resolved and exceptionally well-preserved archive of the Younger Dryas (YD) climate variation. This provides a unique opportunity for detailed investigation of lake system responses during periods of rapid climate cooling (YD onset) and warming (YD termination). The new varve record of Lake Goscia(z) over dot presented here spans 1662 years from the late Allerod (AL) to the early Preboreal (PB). Microscopic varve counting provides an independent chronology with a YD duration of 1149+14/-22 years, which confirms previous results of 1140 +/- 40 years. We link stable oxygen isotopes and chironomid-based air temperature reconstructions with the response of various geochemical and varve microfacies proxies especially focusing on the onset and termination of the YD. Cooling at the YD onset lasted similar to 180 years, which is about a century longer than the terminal warming that was completed in similar to 70 years. During the AL/YD transition, environmental proxy data lagged the onset of cooling by similar to 90 years and revealed an increase of lake productivity and internal lake re-suspension as well as slightly higher detrital sediment input. In contrast, rapid warming and environmental changes during the YD/PB transition occurred simultaneously. However, initial changes such as declining diatom deposition and detrital input occurred already a few centuries before the rapid warming at the YD/PB transition. These environmental changes likely reflect a gradual increase in summer air temperatures already during the YD. Our data indicate complex and differing environmental responses to the major climate changes related to the YD, which involve different proxy sensitivities and threshold processes.Peer reviewe
Completion of neuronal remodeling prompts myelination along developing motor axon branches
Neuronal remodeling and myelination are two fundamental processes during neurodevelopment. How they influence each other remains largely unknown, even though their coordinated execution is critical for circuit function and often disrupted in neuropsychiatric disorders. It is unclear whether myelination stabilizes axon branches during remodeling or whether ongoing remodeling delays myelination. By modulating synaptic transmission, cytoskeletal dynamics, and axonal transport in mouse motor axons, we show that local axon remodeling delays myelination onset and node formation. Conversely, glial differentiation does not determine the outcome of axon remodeling. Delayed myelination is not due to a limited supply of structural components of the axon–glial unit but rather is triggered by increased transport of signaling factors that initiate myelination, such as neuregulin. Further, transport of promyelinating signals is regulated via local cytoskeletal maturation related to activity-dependent competition. Our study reveals an axon branch–specific fine-tuning mechanism that locally coordinates axon remodeling and myelination
Completion of neuronal remodeling prompts myelination along developing motor axon branches
Neuronal remodeling and myelination are two fundamental processes during neurodevelopment. How they influence each other remains largely unknown, even though their coordinated execution is critical for circuit function and often disrupted in neuropsychiatric disorders. It is unclear whether myelination stabilizes axon branches during remodeling or whether ongoing remodeling delays myelination. By modulating synaptic transmission, cytoskeletal dynamics, and axonal transport in mouse motor axons, we show that local axon remodeling delays myelination onset and node formation. Conversely, glial differentiation does not determine the outcome of axon remodeling. Delayed myelination is not due to a limited supply of structural components of the axon-glial unit but rather is triggered by increased transport of signaling factors that initiate myelination, such as neuregulin. Further, transport of promyelinating signals is regulated via local cytoskeletal maturation related to activity-dependent competition. Our study reveals an axon branch-specific fine-tuning mechanism that locally coordinates axon remodeling and myelination
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