273 research outputs found
Global Changes in Scholarly Communication
For more than a decade, the cost of print and electronic journals, particularly in the sciences, has increased rapidly at the same time that the amount of research being reported via published articles has grown exponentially. With academic libraries being less and less able to purchase the journals needed for their communities, the use of the term scholarly communication has evolved to illustrate the breakdown of the process of traditional scholarly publication; that is, as a means to disseminate research results, the present system of scholarly communication can no longer meet the needs of the scholarly community at large.
When looking closely at the term scholarly communication, it has a somewhat broader
meaning than publication, as it also includes the processes by which scholars communicate with one another as they create new knowledge and by which they measure its worth with colleagues prior to making a formal article available to the broader community. For the purposes of this paper we are dividing the scholarly ommunication process into three distinct aspects: 1) the process of conducting research, developing
ideas, and communicating informally with other scholars and scientists; 2) the process of preparing, shaping, and communicating to a group of colleagues what will become formal
research results; and 3) the ultimate formal product that is distributed to libraries and
others in print or electronically. In addition to describing each of these aspects, we will
illustrate some of the changes which are destabilizing longstanding traditions
The Digital Library: a Biography
The idea for the study took shape in a New York City steakhouse where four DLF directors met to reflect on the new roles and responsibilities that were emerging for their libraries as they entered an increasingly networked digital age.1 Realizing that lessons from the past were easier and perhaps more predictive than prognostications about the future, they suggested that a study of DLF member programs would reveal the history, aims, organization, and immediate challenges in their libraries The study progressed quickly, following the development of a lengthy (104-question) survey that was received and completed without complaint at DLF member institutions. We learned subsequently that numerous hands had to be called into play to supply the answers to the questions we posed. Once compiled, the data provided a rich source of information that indicated the very different developmental trajectories and experiences in DLF institutions. Review by a slightly broader group of library directors suggested that the study be extended to include the case studies that are presented here.2 These, they argued, would breathe the life of human experience into otherwise dry, if informative, statistical data. The research was destined from this point to impose even more heavily on already overcrowded schedules that were opened graciously and with the utmost concern for congenial hospitality to accommodate the authors’ site visits
Contribution of NADPH Oxidase to Membrane CD38 Internalization and Activation in Coronary Arterial Myocytes
The CD38-ADP-ribosylcyclase-mediated Ca2+ signaling pathway importantly contributes to the vasomotor response in different arteries. Although there is evidence indicating that the activation of CD38-ADP-ribosylcyclase is associated with CD38 internalization, the molecular mechanism mediating CD38 internalization and consequent activation in response to a variety of physiological and pathological stimuli remains poorly understood. Recent studies have shown that CD38 may sense redox signals and is thereby activated to produce cellular response and that the NADPH oxidase isoform, NOX1, is a major resource to produce superoxide (O2·−) in coronary arterial myocytes (CAMs) in response to muscarinic receptor agonist, which uses CD38-ADP-ribosylcyclase signaling pathway to exert its action in these CAMs. These findings led us hypothesize that NOX1-derived O2·− serves in an autocrine fashion to enhance CD38 internalization, leading to redox activation of CD38-ADP-ribosylcyclase activity in mouse CAMs. To test this hypothesis, confocal microscopy, flow cytometry and a membrane protein biotinylation assay were used in the present study. We first demonstrated that CD38 internalization induced by endothelin-1 (ET-1) was inhibited by silencing of NOX1 gene, but not NOX4 gene. Correspondingly, NOX1 gene silencing abolished ET-1-induced O2·− production and increased CD38-ADP-ribosylcyclase activity in CAMs, while activation of NOX1 by overexpression of Rac1 or Vav2 or administration of exogenous O2·−significantly increased CD38 internalization in CAMs. Lastly, ET-1 was found to markedly increase membrane raft clustering as shown by increased colocalization of cholera toxin-B with CD38 and NOX1. Taken together, these results provide direct evidence that Rac1-NOX1-dependent O2·− production mediates CD38 internalization in CAMs, which may represent an important mechanism linking receptor activation with CD38 activity in these cells
Effects of variation in exercise training load on cognitive performances and neurotrophic biomarkers in patients with coronary artery disease
This study compared the effects of linear (LP) and nonlinear (NLP) training periodization on cognitive functions, neurotrophic biomarkers [plasma brain-derived neurotrophic factor (BDNF), insulin-like growth factor-1 (IGF-1)], and cathepsin-B in patients with coronary artery disease (CAD). Forty-four patients with CAD reported to our laboratory on two occasions to undergo testing procedures before and after training sessions, and were then blindly randomized to NLP or LP for 36 training sessions. Visit 1 included blood samples and a maximal cardiopulmonary exercise testing to get maximal oxygen uptake (V̇o2peak). Visit 2 included cognitive functions assessment. Thirty-nine patients completed the study (LP: n = 20, NLP: n = 19), with no observed changes in cognitive performances after the training intervention in either group. IGF-1 concentration decreased in both groups (time-effect: P < 0.001), whereas BDNF concentration increased (time-effect: P < 0.05) without group interaction, and cathepsin-B did not change after the intervention. Associations were found between ΔV̇o2peak and ΔBDNF (R2 = 0.18, P = 0.04), and ΔIGF-1 and Δshort-term/working memory (R2 = 0.17, P = 0.01) in the pooled sample, with ΔIGF-1 and ΔBDNF accounting for 10% of the variance in Δshort-term/working memory. In the LP group, associations were found between ΔV̇o2peak and ΔBDNF (R2 = 0.45, P = 0.02), ΔBDNF and Δshort-term/working memory (R2 = 0.62, P = 0.004), ΔIGF-1 and Δshort-term/working memory (R2 = 0.31, P = 0.01), and ΔIGF-1 and Δexecutive function (R2 = 0.22, P = 0.04). This study indicates that linear and nonlinear training periodization led to an increase in BDNF, and a decrease in IGF-1, without change in cognitive function in individuals with stable CAD.NEW & NOTEWORTHY We used a novel and supervised iso-energetic training, integrating both moderate- and high-intensity aerobic exercises. Our findings indicate that greater variation in training load did not yield cognitive enhancements, although both protocols exhibited positive effects on brain-derived neurotrophic factor (BDNF) levels. Moreover, this study establishes a clear positive association between short-term and working memory and neurotrophic biomarkers. In addition, the independent predictive value of change in insulin-like growth factor-1 (IGF-1) on improvement in short-term and working memory highlight the close relationship between neurotrophic markers and cognition. Consequently, our results advocate for exercise training interventions targeting neurotrophic biomarkers to enhance cognitive function among individuals with coronary artery disease
Effects of long-term active immunization with the second extracellular loop of human β1- or β3-adrenoceptors in thoracic aorta and mesenteric arteries in Lewis rats
Objective
To evaluate whether active immunization producing β1- or β3-antibodies (β1-ABs and β3-ABs) detected in sera of patients with dilated cardiomyopathies has deleterious effects on vascular reactivity in Lewis rat thoracic aorta (TA) and small mesenteric arteries (SMA).
Design and method
Lewis rats were immunized for 6 months with peptidic sequences corresponding to the second extracellular loop of β1- and β3-adrenoceptors (ARs). During the immunization, systolic blood pressure (SBP) was monitored using the tail cuff method. The vascular reactivity of immunized rats was assessed by ex vivo studies on SMA and TA using various β-AR agonists, phenylephrine and KCl.
Results
The immunizations producing functional β1-ABs and β3-ABs did not affect the SBP. However, in TA from β1-AR-immunized rats, the relaxations mediated by dobutamine and salbutamol were significantly impaired in comparison with adjuvant rats whereas nebivolol-induced relaxation was not modified. Moreover, phenylephrine and KCl-mediated contractions were enhanced in these rats. In contrast, immunization with β3-AR peptide led to the increase of relaxations induced by dobutamine in TA but did not change those induced by salbutamol and nebivolol. Surprisingly, in SMA from both rats immunized with β1- or β3-peptides, relaxations induced by the various β-agonists were not changed whereas phenylephrine and KCl-mediated contractions were impaired.
Conclusions
Our study shows that β1- and β3-ABs can affect vascular reactivity. β1-ABs would have a pathogenic action whereas β3-ABs would have a beneficial effect on aorta reactivity.
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Endothelium-derived endothelin-1
One year after the revelation by Dr. Furchgott in 1980 that the endothelium was obligatory for acetylcholine to relax isolated arteries, it was clearly shown that the endothelium could also promote contraction. In 1988, Dr. Yanagisawa’s group identified endothelin-1 (ET-1) as the first endothelium-derived contracting factor. The circulating levels of this short (21-amino acid) peptide were quickly determined in humans, and it was reported that, in most cardiovascular diseases, circulating levels of ET-1 were increased, and ET-1 was then tagged as “a bad guy.” The discovery of two receptor subtypes in 1990, ET(A) and ET(B), permitted optimization of the first dual ET-1 receptor antagonist in 1993 by Dr. Clozel’s team, who entered clinical development with bosentan, which was offered to patients with pulmonary arterial hypertension in 2001. The revelation of Dr. Furchgott opened a Pandora’s box with ET-1 as one of the actors. In this brief review, we will discuss the physiological and pathophysiological role of endothelium-derived ET-1 focusing on the regulation of the vascular tone, and as much as possible in humans. The coronary bed will be used as a running example in this review because it is the most susceptible to endothelial dysfunction, but references to the cerebral and renal circulation will also be made. Many of the cardiovascular complications associated with aging and cardiovascular risk factors are initially attributable, at least in part, to endothelial dysfunction, particularly dysregulation of the vascular function associated with an imbalance in the close interdependence of nitric oxide and ET-1
Start-to-end simulations of plasma-wakefield acceleration using the MAX IV Linear Accelerator
Plasma-wakefield acceleration (PWFA) relies on the interaction between intense particle bunches and plasma for reaching higher accelerating gradients than what is possible with conventional radio-frequency technology. Using ultra-relativistic beam drivers allows for long acceleration lengths and have potential applications such as energy booster stages for synchrotron light sources or linear colliders and generating ultra-high-brightness beams from the background plasma. In this article, we present start-to-end simulations of the MAX IV Linear Accelerator as part of our investigations into the feasibility of using the linac for a PWFA experiment. We find that PWFA appears to be a viable application for the linac. A part of this conclusion is based on our finding that the general properties of the bunch compressor type employed in the MAX IV linac are well-suited for efficient generation of PWFA-optimized bunch current profiles, both for single- and double-bunch beams
Reporting randomised clinical trials of analgesics after traumatic or orthopaedic surgery is inadequate: a systematic review
Background Several randomised clinical trials (RCTs) of analgesics in postoperative pain after traumatic or orthopaedic surgery (TOS) have been published, but no studies have assessed the quality of these reports. We aimed to examine the quality of reporting RCTs on analgesics for postoperative pain after TOS. Methods Reports of RCTs assessing analgesics in postoperative pain after TOS were systematically searched from electronic databases. The quality of reports was assessed using the CONSORT checklist (scoring range from 0 to 22). The quality was considered poor when scoring was 12 or lesser. The publication year and the impact factor of journals were recorded. Results A total of 92 reports of RCTs were identified and 69 (75%) scored 12 or lesser in CONSORT checklist (range 5-17). The mean (SD) CONSORT score of all reports was 10.6 (2.7). Missing CONSORT items included primary and secondary outcome measures (11%), the specific objectives and hypothesis definition (12%), the sample size calculation (12%), the dates defining the periods of recruitment (12%), the discussion of external validity of findings (14%), the allocation sequence generation (24%), and the interpretation of potential bias or imprecision of results (25%). There was a little improvement in CONSORT scores over time (r = 0.62; p < 0.001) and with impact factor of journals (r = 0.30; p < 0.001). Conclusion Quality of reporting RCTs on analgesics after TOS is poor. Reporting of those RCTs should be improved according to methodological standard checklists in the next years
MAX 4U: an upgrade of the MAX IV 3 GeV ring
The MAX IV 3 GeV storage ring in Lund, Sweden, is the first multibend achromat (MBA) lattice fourth-generation light source worldwide. In order to continue to offer the Swedish and international scientific communities state-of-the-art competitive tools beyond the end of this decade, MAX IV Laboratory launched in 2024 the conceptual design of MAX 4 , an upgrade of its 3 GeV storage ring aiming at an emittance below 100 pm.rad. This performance boost is to be achieved through a minimum-interference upgrade in which localized interventions in selected subsystems and components are carefully chosen to provide the maximum performance increase with minimum cost and, equally important, minimum dark time for the MAX IV user community. This contribution summarises the accelerator physics and engineering aspects of the MAX 4 conceptual design and presents the latest developments
Antispasmodic and vasodilator activities of Morinda citrifolia root extract are mediated through blockade of voltage dependent calcium channels
<p>Abstract</p> <p>Background</p> <p><it>Morinda citrifolia </it>(Noni) is an edible plant with wide range of medicinal uses. It occurs exclusively in tropical climate zone from India through Southeast Asia and Australia to Eastern Polynesia and Hawaii. The objective of this study was to explore the possible mode(s) of action for its antispasmodic, vasodilator and cardio-suppressant effects to rationalize its medicinal use in gut and cardiovascular disorders.</p> <p>Methods</p> <p>Isolated tissue preparations such as, rabbit jejunum, rat and rabbit aorta and guinea pig atria were used to test the antispasmodic and cardiovascular relaxant effects and the possible mode of action(s) of the 70% aqueous-ethanolic extract of <it>Morinda citrifolia </it>roots (Mc.Cr).</p> <p>Results</p> <p>The Mc.Cr produced a concentration-dependent relaxation of spontaneous and high K<sup>+ </sup>induced contractions in isolated rabbit jejunum preparations. It also caused right ward shift in the concentration response curves of Ca<sup>++</sup>, similar to that of verapamil. In guinea-pig right atria, Mc.Cr caused inhibition of both atrial force and rate of spontaneous contractions. In rabbit thoracic aortic preparations, Mc.Cr also suppressed contractions induced by phenylephrine (1.0 μM) in normal- Ca<sup>++ </sup>and Ca<sup>++</sup>-free Kerb's solutions and by high K<sup>+</sup>, similar to that of verapamil. In rat thoracic aortic preparations, Mc.Cr also relaxed the phenylephrine (1.0 μM)-induced contractions. The vasodilatory responses were not altered in the presence of L-NAME (0.1 mM) or atropine (1.0 μM) and removal of endothelium.</p> <p>Conclusions</p> <p>These results suggest that the spasmolytic and vasodilator effects of Mc.Cr root extract are mediated possibly through blockade of voltage-dependent calcium channels and release of intracellular calcium, which may explain the medicinal use of <it>Morinda citrifolia </it>in diarrhea and hypertension. However, more detailed studies are required to assess the safety and efficacy of this plant.</p
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