1,097 research outputs found
Open access self-archiving: An author study
No full textThis, our second author international, cross-disciplinary study on open access had 1296 respondents. Its focus was on self-archiving. Almost half (49%) of the respondent population have self-archived at least one article during the last three years. Use of institutional repositories for this purpose has doubled and usage has increased by almost 60% for subject-based repositories. Self-archiving activity is greatest amongst those who publish the largest number of papers. There is still a substantial proportion of authors unaware of the possibility of providing open access to their work by self-archiving. Of the authors who have not yet self-archived any articles, 71% remain unaware of the option. With 49% of the author population having self-archived in some way, this means that 36% of the total author population (71% of the remaining 51%), has not yet been appraised of this way of providing open access. Authors have frequently expressed reluctance to self-archive because of the perceived time required and possible technical difficulties in carrying out this activity, yet findings here show that only 20% of authors found some degree of difficulty with the first act of depositing an article in a repository, and that this dropped to 9% for subsequent deposits. Another author worry is about infringing agreed copyright agreements with publishers, yet only 10% of authors currently know of the SHERPA/RoMEO list of publisher permissions policies with respect to self-archiving, where clear guidance as to what a publisher permits is provided. Where it is not known if permission is required, however, authors are not seeking it and are self-archiving without it. Communicating their results to peers remains the primary reason for scholars publishing their work; in other words,
researchers publish to have an impact on their field. The vast majority of authors (81%) would willingly comply with a mandate from their employer or research funder to deposit copies of their articles in an institutional or subject-based repository. A further 13% would comply reluctantly; 5% would not comply with such a mandate
The Natural and Un-Natural History of Patients with Scimitar Syndrome: An Italian Multicentric Study
No full textOn exclusive h→Vl+l− decays
No full textWe study a set of exclusive decay modes of the Standard Model Higgs boson into a vector meson and a dilepton pair: h→Vl+l−, with V=Υ,J/ψ,φ, and l=μ,τ, determining the decay rates, the dilepton mass spectra and the V longitudinal helicity fraction distributions. In the same framework, we analyze the exclusive modes into neutrino pairs View the MathML source. We also discuss the implications of the recent CMS and ATLAS results for the lepton flavor-changing process h→τ+μ− on the h→Vτ+μ− decay mode
Nitric oxide formation during cortical spreading depression is critical for rapid subsequent recovery of ionic homeostasis
No full textNoCortical spreading depression (CSD) is a temporary disruption of local ionic homeostasis that propagates slowly across the cerebral cortex. Cortical spreading depression promotes lesion progression in experimental stroke, and may contribute to the initiation of migraine attacks. The purpose of this study was to investigate the roles of the marked increase of nitric oxide (NO) formation that occurs with CSD. Microdialysis electrodes were implanted in the cortex of anesthetized rats to perform the following operations within the same region: (1) elicitation of CSD by perfusion of high K+ medium; (2) recording of CSD elicitation; (3) application of the NO synthase inhibitor, NG-nitro-L-arginine methyl ester (L-NAME); and (4) recording of dialysate pH changes. The primary effect of L-NAME (0.3 to 3.0 mmol/L in the perfusion medium) was a marked widening of individual CSD wave, resulting essentially from a delayed initiation of the repolarization phase. This change was due to NO synthase inhibition because it was not observed with the inactive isomer D-NAME, and was reversed by L-arginine. This effect did not appear to be linked to the suppression of a sustained, NO-mediated vascular change associated with the superposition of NO synthase inhibition on high levels of extracellular K+. The delayed initiation of repolarization with local NO synthase inhibition may reflect the suppression of NO-mediated negative feedback mechanisms acting on neuronal or glial processes involved in CSD genesis. However, the possible abrogation of a very brief, NO-mediated vascular change associated with the early phase of CSD cannot be ruled out
Tolerable degree of muscle sacrifice when harvesting a vastus lateralis or myocutaneous anterolateral thigh flap
No full textThe myocutaneous anterolateral thigh (ALT) and vastus lateralis (VL) flaps include a large muscle mass and a sufficient vascular pedicle, and they have been used for decades to reconstruct traumatic and acquired defects of the head and neck and extremities. In spite of these benefits, musculoskeletal dysfunction was reported in nearly 1 out of 20 patients at follow-up. It is unclear whether the recently proposed muscle-sparing flap-raising approach could preserve VL muscle function and whether patients at increased risk could benefit from such an approach. Therefore, we performed a predictive dynamic gait simulation based on a biological motion model with gradual weakening of the VL during a self-selected and fast walking speed to determine the compensable degree of VL muscle reduction. Muscle force, joint angle, and joint moment were measured. Our study showed that VL muscle reduction could be compensated up to a certain degree, which could explain the observed incidence of musculoskeletal dysfunction. In elderly or fragile patients, the VL muscle should not be reduced by 50% or more, which could be achieved by muscle-sparing flap-raising of the superficial partition only. In young or athletic patients, a VL muscle reduction of 10%, which corresponds to a muscle cuff, has no relevant effect. Yet, a reduction of more than 30% leads to relevant weakening of the quadriceps. Therefore, in this patient population with the need for a large portion of muscle, alternative flaps should be considered. This study can serve as the first basis for further investigations of human locomotion after flap-raising.Green Open Access added to TU Delft Institutional Repository 'You share, we take care!' - Taverne project https://www.openaccess.nl/en/you-share-we-take-care Otherwise as indicated in the copyright section: the publisher is the copyright holder of this work and the author uses the Dutch legislation to make this work public.Biomechatronics & Human-Machine Contro
Apoptosis-inducing factor is involved in the regulation of caspase-independent neuronal cell death
No full textCaspase-independent death mechanisms have been shown to execute apoptosis in many types of neuronal injury. P53 has been identified as a key regulator of neuronal cell death after acute injury such as DNA damage, ischemia, and excitotoxicity. Here, we demonstrate that p53 can induce neuronal cell death via a caspase-mediated process activated by apoptotic activating factor-1 (Apaf1) and via a delayed onset caspase-independent mechanism. In contrast to wild-type cells, Apaf1-deficient neurons exhibit delayed DNA fragmentation and only peripheral chromatin condensation. More importantly, we demonstrate that apoptosis-inducing factor (AIF) is an important factor involved in the regulation of this caspase-independent neuronal cell death. Immunofluorescence studies demonstrate that AI F is released from the mitochondria by a mechanism distinct from that of cytochrome-c in neurons undergoing p53-mediated cell death. The Bcl-2 family regulates this release of AIF and subsequent caspase-independent cell death. In addition, we show that enforced expression of AIF can induce neuronal cell death in a Bax- and caspase-independent manner. Microinjection of neutralizing antibodies against AIF significantly decreased injury-induced neuronal cell death in Apaf1-deficient neurons, indicating its importance in caspase-independent apoptosis. Taken together, our results suggest that AIF may be an important therapeutic target for the treatment of neuronal injury
Figure 6 in Unmasking Aurelia species in the Mediterranean Sea: an integrative morphometric and molecular approach
No full textFigure 6. Ontogenetic variation in subgenital pore size (f11) and position (f12) in male specimens of Aurelia coerulea from: A, Empuriabrava Harbour (EH), bell diameter (BD) = 63 mm; B, Varano Lagoon (VL), BD = 120 mm.Published as part of Scorrano, Simonetta, Aglieri, Giorgio, Boero, Ferdinando, Dawson, Michael N. & Piraino, Stefano, 2017, Unmasking Aurelia species in the Mediterranean Sea: an integrative morphometric and molecular approach, pp. 243-267 in Zoological Journal of the Linnean Society 180 (5) on page 254, DOI: 10.1111/zoj.12494, http://zenodo.org/record/571098
The chaperone activity of heat shock protein 90 is critical for maintaining the stability of leucine-rich repeat kinase 2.
No full textLRRK2 affects vesicle trafficking, neurotransmitter extracellular level and membrane receptor localization
No full text""The leucine-rich repeat kinase 2 (LRRK2) gene was found to play a role in the pathogenesis of both familial and sporadic Parkinson's disease (PD). LRRK2 encodes a large multi-domain protein that is expressed in different tissues. To date, the physiological and pathological functions of LRRK2 are not clearly defined. In this study we have explored the role of LRRK2 in controlling vesicle trafficking in different cellular or animal models and using various readouts. In neuronal cells, the presence of LRRK2(G2019S) pathological mutant determines increased extracellular dopamine levels either under basal conditions or upon nicotine stimulation. Moreover, mutant LRRK2 affects the levels of dopamine receptor D1 on the membrane surface in neuronal cells or animal models. Ultrastructural analysis of PC12-derived cells expressing mutant LRRK2(G2019S) shows an altered intracellular vesicle distribution. Taken together, our results point to the key role of LRRK2 to control vesicle trafficking in neuronal cells. "
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