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Search Results: 1 - 10 of 168761 matches for " Alisa E. Shaw "
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A Genetically Encoded Reporter for Real-Time Imaging of Cofilin-Actin Rods in Living Neurons
Jianjie Mi, Alisa E. Shaw, Chi W. Pak, Keifer P. Walsh, Laurie S. Minamide, Barbara W. Bernstein, Thomas B. Kuhn, James R. Bamburg
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0083609
Abstract: Filament bundles (rods) of cofilin and actin (1:1) form in neurites of stressed neurons where they inhibit synaptic function. Live-cell imaging of rod formation is hampered by the fact that overexpression of a chimera of wild type cofilin with a fluorescent protein causes formation of spontaneous and persistent rods, which is exacerbated by the photostress of imaging. The study of rod induction in living cells calls for a rod reporter that does not cause spontaneous rods. From a study in which single cofilin surface residues were mutated, we identified a mutant, cofilinR21Q, which when fused with monomeric Red Fluorescent Protein (mRFP) and expressed several fold above endogenous cofilin, does not induce spontaneous rods even during the photostress of imaging. CofilinR21Q-mRFP only incorporates into rods when they form from endogenous proteins in stressed cells. In neurons, cofilinR21Q-mRFP reports on rods formed from endogenous cofilin and induced by all modes tested thus far. Rods have a half-life of 30–60 min upon removal of the inducer. Vesicle transport in neurites is arrested upon treatments that form rods and recovers as rods disappear. CofilinR21Q-mRFP is a genetically encoded rod reporter that is useful in live cell imaging studies of induced rod formation, including rod dynamics, and kinetics of rod elimination.
Amyloid-β and Proinflammatory Cytokines Utilize a Prion Protein-Dependent Pathway to Activate NADPH Oxidase and Induce Cofilin-Actin Rods in Hippocampal Neurons
Keifer P. Walsh, Laurie S. Minamide, Sarah J. Kane, Alisa E. Shaw, David R. Brown, Bruce Pulford, Mark D. Zabel, J. David Lambeth, Thomas B. Kuhn, James R. Bamburg
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0095995
Abstract: Neurites of neurons under acute or chronic stress form bundles of filaments (rods) containing 1:1 cofilin:actin, which impair transport and synaptic function. Rods contain disulfide cross-linked cofilin and are induced by treatments resulting in oxidative stress. Rods form rapidly (5–30 min) in >80% of cultured hippocampal or cortical neurons treated with excitotoxic levels of glutamate or energy depleted (hypoxia/ischemia or mitochondrial inhibitors). In contrast, slow rod formation (50% of maximum response in ~6 h) occurs in a subpopulation (~20%) of hippocampal neurons upon exposure to soluble human amyloid-β dimer/trimer (Aβd/t) at subnanomolar concentrations. Here we show that proinflammatory cytokines (TNFα, IL-1β, IL-6) also induce rods at the same rate and within the same neuronal population as Aβd/t. Neurons from prion (PrPC)-null mice form rods in response to glutamate or antimycin A, but not in response to proinflammatory cytokines or Aβd/t. Two pathways inducing rod formation were confirmed by demonstrating that NADPH-oxidase (NOX) activity is required for prion-dependent rod formation, but not for rods induced by glutamate or energy depletion. Surprisingly, overexpression of PrPC is by itself sufficient to induce rods in over 40% of hippocampal neurons through the NOX-dependent pathway. Persistence of PrPC-dependent rods requires the continuous activity of NOX. Removing inducers or inhibiting NOX activity in cells containing PrPC-dependent rods causes rod disappearance with a half-life of about 36 min. Cofilin-actin rods provide a mechanism for synapse loss bridging the amyloid and cytokine hypotheses for Alzheimer disease, and may explain how functionally diverse Aβ-binding membrane proteins induce synaptic dysfunction.
Vasculopathy and disordered angiogenesis in selected rheumatic diseases: rheumatoid arthritis and systemic sclerosis
Alisa E Koch, Oliver Distler
Arthritis Research & Therapy , 2007, DOI: 10.1186/ar2187
Abstract: Angiogenesis, the process of new blood vessel formation, is controlled by a subtle balance between endogenous stimulators, which induce blood vessel growth, and inhibitors, which prevent growth. In processes such as wound healing, angiogenesis is a well programmed cascade of events that comprises a number of distinct steps. Angiogenic stimuli activate endothelial cells, which produce proteolytic enzymes that degrade the basement membrane and the perivascular extracellular matrix. Endothelial cells proliferate and migrate into the perivascular area, forming 'primary sprouts'. Subsequent lumenation of these primary sprouts leads to formation of capillary loops, which is followed by synthesis of a new basement membrane and blood vessel maturation to complete tube-like structures through which blood can flow [1] (Figure 1).Like any biological system, inducers of angiogenesis are counterbalanced by inhibitors. However, in angiogenesis the inhibitors often outweigh the inducers, resulting in a normal physiological balance. When the converse situation occurs, conditions characterized by angiogenesis, such as inflammatory angiogenesis or angiogenesis related to tumour growth, can develop. In this review we explore potential initiators of vascular injury in two example inflammatory rheumatic diseases, namely rheumatoid arthritis (RA) and scleroderma (systemic sclerosis [SSc]), in which the angiogenic process appears to be disrupted very differently. We also discuss how the angiogenic process might be manipulated for therapeutic benefit in the treatment of these debilitating diseases.The rheumatic diseases are a family of closely related disorders that includes RA, SSc and systemic lupus erythematosus. RA is characterized by excessive angiogenesis [2] and it has been studied extensively in this regard.Proangiogenic mediators associated with RA include the following (Table 1): growth factors such as vascular endothelial growth factor (VEGF); cytokines such as tumour necrosis f
Endothelial cells and immune cell migration
Zoltan Szekanecz, Alisa E Koch
Arthritis Research & Therapy , 2000, DOI: 10.1186/ar114
Abstract: Leukocyte extravasation through the endothelial barrier is important in the pathogenesis of inflammatory disorders such as rheumatoid arthritis (RA). Endothelial cells line the lumina of vessels, thus separating and also connecting the blood and the synovial tissue. It has become clear that, in inflammation, endothelial cells are not only passive bystanders but are active responders to various stimuli (state of activation of leukocytes, exogenous cytokines, endogenous endothelial mediators, and crosstalk between adhesion molecules). Thus endothelia are targets for inflammatory leukocytes and their mediators. In return, endothelial cells themselves produce a number of inflammatory mediators, express cellular adhesion molecules (CAMs) and therefore directly influence the action of leukocytes and the outcome of the inflammatory response [1,2].Endothelial cells are involved in a number of mechanisms underlying arthritis. Various inflammatory mediators, primarily pro-inflammatory cytokines including tumor necrosis factor (TNF)-α and IL-1β, activate endothelial cells. In response, there is an upregulation of endothelial CAMs in RA, leading to increased leukocyte-endothelial interactions [2,3,4].In this review we discuss the role of endothelial cells, as well as that of leukocyte-endothelial adhesion and migration in synovial inflammation. First we describe the general characteristics of leukocyte-endothelial adhesion. Then the role of the most relevant CAMs, as well as that of the most important adhesive pathways determined by these CAMs in arthritis is introduced. Finally we discuss potential strategies of targeting these mechanisms.The ingress of leukocytes into the synovium is an active process mediated by a number of CAMs. The cascade of events begins with the adhesion of neutrophils, lymphocytes and monocytes to the specialized, fenestrated synovial endothelium [4,5]. High endothelial venule (HEV)-like microvessels, similar to HEVs in the primary lymphoid organs, are
Vascular involvement in rheumatic diseases: 'vascular rheumatology'
Zoltán Szekanecz, Alisa E Koch
Arthritis Research & Therapy , 2008, DOI: 10.1186/ar2515
Abstract: Vessels and the vascular endothelium are involved in the pathogenesis of inflammatory rheumatic diseases. Rheumatoid arthritis (RA) serves as a prototype of these diseases as it is the most common type of arthritis and a great body of data is available regarding leukocyte recruitment into the synovium, angiogenesis, and accelerated atherosclerosis. The term 'vascular rheumatology' has been accepted by many investigators and includes both microvascular and macrovascular involvement in rheumatic diseases. Apart from RA, systemic lupus erythematosus (SLE), systemic sclerosis (SSc), the antiphospholipid syndrome (APS), and systemic vasculitides have been associated with vascular inflammation, altered angiogenesis, and increased cardiovascular morbidity and mortality. In this review, we will discuss the most relevant information on arthritis-related vascular inflammation, including the role of endothelial cells (ECs), endothelial adhesion molecules (CAMs) and chemokines, as well as the involvement of neovascularization and some aspects of accelerated atherosclerosis in rheumatic diseases. We will discuss RA in more detail, and other connective tissue diseases described above will also be mentioned. Finally, some aspects of vascular targeting in rheumatology will also be briefly summarized.In arthritis, leukocyte ingress into the synovium occurs by leukocyte adhesion to ECs and then by transendothelial migration [1-8]. The chemotaxis of these leukocytes is regulated mainly by various chemokines [1,8-14]. Several CAMs have been implicated in leukocyte-EC interactions [1-4,7,8]. ECs play an active role in inflammation. Synovitis is associated with vasodilation and increased endothelial permeability (leakage) and vascular injury followed by endothelial regeneration [4-6]. ECs secrete several vasodilatory mediators, including nitric oxide, prostacyclin (PGI2), platelet-activating factor, histamine, and others [4-6]. Increased vascular permeability associated with EC retractio
Vasculogenesis in rheumatoid arthritis
Zoltán Szekanecz, Alisa E Koch
Arthritis Research & Therapy , 2010, DOI: 10.1186/ar2943
Abstract: Endothelial progenitor cells (EPCs) are hematopoietic stem cells expressing CD34, CD133, type 2 vascular endothelial growth factor (VEGF) receptor (VEGFR-2 or Flk-1), and the CXCR4 chemokine receptor [1-4]. During vasculogenesis, EPCs are mobilized from the bone marrow and they differentiate into mature endothelial cells [3]. Under normal conditions, vasculogenesis is involved in both prenatal and postnatal tissue development, vascular repair, and atherosclerosis [2,3].In rheumatoid arthritis (RA), several groups have described defective vasculogenesis related to impaired EPC numbers and functions in RA [4-6]. Impaired vasculogenesis has been associated with increased cardiovascular morbidity and mortality in RA [7,8]. Effective antirheumatic therapy, such as corticosteroids and tumor necrosis factor-alpha (TNF-α) blockers, may stimulate the outgrowth and function of EPCs and thus may restore defective vasculogenesis in arthritis [5]. In addition, as the induction of vasculogenesis may be beneficial for patients with cardiovascular disease [8], the stimulation of EPCs and vasculogenesis may also suppress premature atherosclerosis underlying RA [7].In the previous issue of Arthritis Research & Therapy, Jodon de Villeroché and colleagues [1] assessed late-outgrowth EPCs in RA and found increased colony-formation capacity of these cells in RA. Furthermore, higher or lower EPC numbers correlated with active disease and disease in remission, respectively. These results seem to be somewhat controversial as a number of other investigators reported defective EPC function in RA and lower EPC numbers in active RA [5,6]. There has been only one report by the same group, Allanore and colleagues [9], suggesting that circulating EPC numbers may be higher in RA. Nevertheless, Jodon de Villeroché and colleagues [1] conducted an approach that was significantly different from that of others. Instead of analyzing all EPCs, they differentiated two EPC sub-populations, namely EPCs of mo
Lesson Planning in Primary School Using Lesson Study and Open Approach  [PDF]
Alisa Moonsri, Auijit Pattanajak
Psychology (PSYCH) , 2013, DOI: 10.4236/psych.2013.412155

Lesson plans are generally written in a way that helps teachers to layout and run classroom activities. Many researchers have examined how teachers go about planning. This clearly shows that instructional plans play a central role in teaching and creating effective learning environments (Clark & Dunn, 1991; Reiser & Dick, 1996; Shauelson, 1983 cited in Koszalka et al., 1999). In context of school using lesson study and open approach followed conception of Inprasitha (2010), the importance of lesson study processes is collaborative lesson planning. After that the teachers who participate in lesson study group use these lesson plans in the classroom, observe and collect students’ thought and learning processes. And in planning the lessons use problems that students encounter in everyday life, so as to stimulate students to work to achieve the objective (Fernandez & Yoshida, 2004). The data were collected by video and audio recording while the target group were planning and teaching the lessons in lesson study process, then were transcribed to the protocol and analyzed by using theoretical framework of Stigler and Hiebert (1999). The research revealed that the target group discussed during the lesson planning process detailing about exact words, problem situations, materials, the anticipated solutions, students’ thoughts and responses, time used in each part of the lesson, and how to summarize the lesson. In the lesson planning, the exact words used in the problem situations were mostly mentioned. Moreover, in lesson planning, the issue of details of introduction design was discussed a lot. There were some issues which were not discussed during the teachers-included designing of the lesson plan. However, they were discussed while the teacher was using the lesson plan in class during instructional management.

Sex steroids do not affect shigatoxin cytotoxicity on human renal tubular or glomerular cells
Alisa K Hughes, Douglas I Schmid, Donald E Kohan
BMC Nephrology , 2002, DOI: 10.1186/1471-2369-3-6
Abstract: Cultured human glomerular endothelial (HGEN), human glomerular visceral epithelial (HGEC) and human proximal tubule (HPT) cells were exposed to Stx-1 after pre-incubation with progesterone, β-estradiol or testosterone followed by determination of cytotoxicity.Under basal conditions, Stx-1 potently and dose-dependently killed HPT and HGEC, but had relatively little effect on HGEN. Pre-incubation for 1, 2 or 7 days with physiologic or pharmacologic concentrations of progesterone, β-estradiol or testosterone had no effect on Stx-1 cytotoxicity dose-response on any cell type. In addition, no steroid altered Gb3 expression (Stx receptor) by any cell type at any time point.These data do not support the notion that hormonal changes associated with puberty induce an Stx-resistant state within kidney cells.The factors responsible for the age-related incidence of post-diarrheal hemolytic uremic syndrome (HUS) are unknown. Clinical data indicate that the peak incidence of HUS occurs around two years of age, but the disease clearly occurs in significant numbers of older children [1]. Population-based studies suggest that there is a decline in the incidence of HUS from a peak at age 1–2 years until a nadir at about age 11 years [1,2]. In addition, a case-control study of the Washington State outbreak of HUS revealed that the mean age of patients with HUS was 8 years, while the mean age of patients without HUS was 15 years [3]. These studies raise the possibility, therefore, that the appearance or disappearance of a factor or factors in adolescents and adults reduces susceptibility to end-organ injury in HUS.HUS is thought to be due, at least in large part, to Shiga toxin (Stx)-mediated cell toxicity [4]. Since the kidney is a primary target of Stx in patients with HUS, it has been hypothesized that the preferential renal injury occurring in children with HUS is related to heightened renal susceptibility to Stx in this age group. Such increased renal sensitivity to Stx in childre
Nancy E. McIntyre,Richard A. Nisbett,Alisa Abuzeineh,Tyla Holsomback
Mastozoolog?-a neotropical , 2009,
Abstract: Durante dos a os consecutivos (marzo 2002 a agosto del 2003), estudiamos la ecología básica de Oryzomys palustris, el reservorio natural de la cepa Bayou de Hantavirus, bajo la hipótesis de que el estado serológico afectaba dos variables demográficas: el tama o del ámbito de hogar (home range) y el uso de hábitat. Encontramos asociaciones significativas entre uso del macrohábitat y el estado serológico, pero no se encontraron diferencias en el uso del microhabitat entre entre animales seropositivos y seronegativos. Sin embargo, machos adultos serológicamente positivos tuvieron ámbitos de hogar más amplios que los seronegativos, además de ser más grandes en términos de masa corporal y tama o de sus testículos. Sugerimos que estos patrones pueden reflejar la influencia de la infección sobre la ecología de roedores, posiblemente en función de dominancia social y acceso a hábitats preferidos.
Shaping the future of integrated care: what can we learn from history?
Benedict Rumbold,Sara E. Shaw
International Journal of Integrated Care , 2010,
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