2,391 research outputs found
The impact of physical processes on algal growth
Mixing and transport processes in surface waters strongly influence the structure of aquatic ecosystems. The impact of mixing on algal growth is species-dependent, affecting the competition among species and acting as a selective factor for the composition of the biocoenose. Were it not for the ever-changing ”aquatic weather”, the composition of pelagic ecosystems would be relatively simple. Probably just a few optimally adapted algal species would survive in a given water-body. In contrast to terrestrial ecosystems, in which the spatial heterogeneity is primarily responsible for the abundance of niches, in aquatic systems (especially in the pelagic zone) the niches are provided by the temporal structure of physical processes. The latter are discussed in terms of the relative sizes of physical versus biological time-scales. The relevant time-scales of mixing and transport cover the range between seconds and years. Correspondingly, their influence on growth of algae is based on different mechanisms: rapid changes are relevant for the fast biological processes such as nutrient uptake and photosynthesis, and the slower changes are relevant for the less dynamic processes such as growth, respiration, mineralization, and settling of algal cells. Mixing time-scales are combined with a dynamic model of photosynthesis to demonstrate their influence on algal growth
Functional Assessment of Heart Failure Patients
Heart failure (HF) is the condition characterized by the inability of the heart to pump sufficient blood to meet the demands of the body. It has been well established that both the prevalence and incidence of HF is increasing.1 There are 2 primary types of HF, categorized by ejection fraction: Reduced ejection fraction and preserved ejection fraction.2 Additionally, HF is commonly classified into stages from mild to severe using a symptom-based scale related to functional limitations.
One of the hallmark features of HF is exercise intolerance, which is accompanied by symptoms of fatigue and shortness of breath.3 As the disease progresses, patients experience a downward spiral as these symptoms typically result in reduced physical activity, which leads to progressively worsening exercise intolerance. Typically, patients with HF are faced with what can be termed a functional disability. Often, their reduced functional abilities restrict or may even prevent them from performing occupational tasks, which may result in loss of work. Additionally, it is well known that patients with HF experience impairment in the ability to carry out activities of daily living and suffer from reduced quality of life.
The objective of this paper was to provide an overview of assessments of functional ability of patients with HF. Two categories of assessment are reviewed: Cardiovascular function and muscular function. The review includes procedural guidance on how to administer the assessments and information related to the advantages and disadvantages of each method. Because both HF types (reduced ejection fraction and preserved ejection fraction) are characterized by exercise intolerance, the procedures can be used effectively with either type of HF
Levels of C-reactive protein associated with high and very high cardiovascular risk are prevalent in patients with rheumatoid arthritis.
ObjectiveC-reactive protein (CRP) levels>3 mg/L and>10 mg/L are associated with high and very high cardiovascular risk, respectively, in the general population. Because rheumatoid arthritis (RA) confers excess cardiovascular mortality, we determined the prevalence of these CRP levels among RA patients stratified on the basis of their RA disease activity.MethodsWe evaluated physician and patient global assessments of disease activity, tender and swollen 28 joint counts, erythrocyte sedimentation rate (ESR), and CRP measured in a single clinic visit for 151 RA patients. Disease activity was calculated using the Clinical Disease Activity Index (CDAI) and the Disease Activity Score 28 Joints (DAS28-ESR and DAS28-CRP).ResultsMedian CRP level was 5.3 mg/L. 68% of patients had CRP>3 mg/L, and 25% had CRP>10 mg/L. Of those with 0-1 swollen joints (n = 56), or 0-1 tender joints (n = 81), 64% and 67%, respectively, had CRP>3 mg/L, and 23% and 20%, respectively, had CRP>10 mg/L. Of those with remission or mildly active disease by CDAI (n = 58), DAS28-ESR (n = 39), or DAS28-CRP (n = 70), 49-66% had CRP>3 mg/L, and 10-14% had CRP>10 mg/L. Of patients with moderate disease activity by CDAI (n = 51), DAS28-ESR (n = 78), or DAS28-CRP (n = 66), 67-73% had CRP>3 mg/L, and 25-33% had CRP>10 mg/L.ConclusionEven among RA patients whose disease is judged to be controlled by joint counts or standardized disease scores, a substantial proportion have CRP levels that are associated high or very high risk for future cardiovascular events in the general population
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The OX-44 molecule couples to signaling pathways and is associated with CD2 on rat T lymphocytes and a natural killer cell line.
The MRC OX-44 molecule, which is expressed on all peripheral leukocytes, identifies the subset of thymocytes capable of proliferating in response to alloantigens and lectins (Paterson, D.J., J.R. Green, W.A. Jefferies, M. Puklavec, and A.F. Williams. 1987. J. Exp. Med. 165:1). When we isolated monoclonal antibodies (mAbs) on the basis of their ability to activate the phosphatidylinositol signaling pathway in RNK-16 cells (a rat leukemia line with natural killer activity), three of the resulting mAbs recognized the OX-44 molecule. Addition of these mAbs to RNK-16 elicits protein tyrosine phosphorylation, generates inositol phosphates, and increases the concentration of cytoplasmic free calcium. These responses require the addition of intact mAb and are not observed with F(ab')2 fragments. One of these mAbs (7D2) is mitogenic for freshly isolated rat splenic T cells and synergizes with a mAb to the T cell antigen receptor in this activation. A 50-60-kD glycoprotein coprecipitates with the OX-44 molecule from RNK-16 cells and rat splenic T cells. Peptide mapping and reprecipitation studies indicate that the coprecipitating molecule is CD2. Thus, the OX-44 molecule can couple to multiple signaling pathways and associates with CD2 on both RNK-16 and rat T cells
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The SH3 domain of p56lck binds to proline-rich sequences in the cytoplasmic domain of CD2.
CD2, a cell surface glycoprotein expressed on T cells and natural killer cells, can couple to signaling pathways that result in T cell proliferation. An Src-like protein tyrosine kinase, p56lck, coprecipitates with CD2, and perturbation of CD2 by monoclonal antibodies results in an increase in the activity of p56lck, suggesting that an interaction with p56lck contributes to CD2-mediated signaling. Herein, we investigate the mechanism by which CD2 associates with p56lck. We demonstrate that CD2 and p56lck associate when coexpressed in nonlymphoid cells, that this association requires the cytoplasmic domain of CD2, and that the SH3 domain of p56lck mediates its interactions with CD2. Using truncation mutants of CD2, we identify two regions in the cytoplasmic domain of CD2 involved in binding p56lck. Each region contains a proline-rich sequence that, in the form of a synthetic peptide, directly binds p56lck. Thus, proline-rich sequences in the cytoplasmic domain of CD2 allow this transmembrane receptor to bind to the SH3 domain of p56lck
Angiotensinergic innervation of rat and human mesenteric resistant blood vessels
In contrast to the current believe that angiotensin II (Ang II) only interacts with the sympathetic nervous system (SNS) as a circulating hormone, we document here the existence of an endogenous renin-angiotensin system (RAS) in the sympathetic coeliac ganglion and the angiotensinergic innervation with mesenteric resistant blood vessels. Our findings indicate that Ang II is synthesized inside the neurons of sympathetic coeliac ganglion and may act as an endogenous neurotransmitter locally on the mesenteric resistant blood vessels
Scientific Publishing: the Dilemma of Research Funding Organisations
Present changes in scientific publishing, especially those summarised by the term ‘Open Access' (OA), may ultimately lead to the complete replacement of a reader-paid to an author, or funding-paid, publication system. This transformation would shift the financial burden for scientific publishing from the Research Performing Organisations (RPOs), particularly from scientific libraries, universities, etc, to the Research Funding Organisations (RFOs). The transition phase is difficult; it leads to double funding of OA publications (by subscriptions and author-sponsored OA) and may thus increase the overall costs of scientific publishing. This may explain why - with a few exceptions - RFOs have not been at the forefront of the OA paradigm in the past. In 2008, the General Assembly of EUROHORCs, the European organisation of the heads of research councils, agreed to recommend to its member organisations at least a minimal standard of Open Access based on the Berlin Declaration of 2003 (green way of OA). In the long run, the publishing system needs some fundamental changes to reduce the present costs and to keep up its potential. In order to design a new system, all players have to cooperate and be ready to throw overboard some old traditions, lovable as they may b
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