Academic literature on the topic 'Edema factor'
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Journal articles on the topic "Edema factor"
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Hirashima, Yutaka, Nakamasa Hayashi, Osamu Fukuda, Hideki Ito, Shunro Endo, and Akira Takaku. "Platelet-activating factor and edema surrounding meningiomas." Journal of Neurosurgery 88, no. 2 (February 1998): 304–7. http://dx.doi.org/10.3171/jns.1998.88.2.0304.
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Object. The purpose of this study was to evaluate the involvement of platelet-activating factor (PAF) in the formation of edema surrounding meningiomas. Methods. Volumes of tumor and peritumoral edema were calculated based on three-dimensional reconstructed magnetic resonance images in 31 patients with intracranial meningiomas. The authors measured tumor concentrations of PAF and localized PAF and leukocytes in the tumors by using immunohistochemical studies. A significant positive correlation was found between peritumoral edema and PAF concentration. Both PAF and leukocyte common antigen were localized to the interstitial tissue of the tumor. Edema production was related to the degree of leukocyte infiltration in meningiomas. Conclusions. It appears that PAF, which may arise from infiltrating leukocytes, is important to the development of peritumoral edema in patients with meningioma.
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Seifert, Roland, and Stefan Dove. "Inhibitors of Bacillus anthracis edema factor." Pharmacology & Therapeutics 140, no. 2 (November 2013): 200–212. http://dx.doi.org/10.1016/j.pharmthera.2013.07.002.
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Chen, Deliang, Milind Misra, Laurie Sower, Johnny W. Peterson, Glen E. Kellogg, and Catherine H. Schein. "Novel inhibitors of anthrax edema factor." Bioorganic & Medicinal Chemistry 16, no. 15 (August 2008): 7225–33. http://dx.doi.org/10.1016/j.bmc.2008.06.036.
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Villeco, June P. "Edema: A Silent but Important Factor." Journal of Hand Therapy 25, no. 2 (April 2012): 153–62. http://dx.doi.org/10.1016/j.jht.2011.09.008.
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Post, Michał, Dorota Polakowska, Dominika Wróbel-Dudzińska, and Jacek P. Szaflik. "Therapeutic Approaches for Treatment of Diabetic Macular Edema." Ophthalmology, no. 3 (December 30, 2023): 26–31. http://dx.doi.org/10.5114/oku/178041.
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Diabetic macular edema is an ocular complication of diabetes mellitus, leading to significant visual impairment. The pathogenesis of diabetic macular edema occurs through the interaction of multiple molecular mediators, including the overexpression of several growth factors, including vascular endothelial growth factor, angiopoietin-1, and -2, insulin-like growth factor-1, etc. These growth factors mediate endothelial cell proliferation, angiogenesis, protease production. Treatment for diabetic macular edema involves primary management of diabetes mellitus, laser photocoagulation, and pharmacotherapeutics targeting mediators, namely, the anti-vascular endothelial growth factor pathway. The introduction of anti-vascular endothelial growth factor therapies has resulted in significant clinical improvements compared to laser photocoagulation alone. However, the presence of anti-vascular endothelial growth factor non-responders and multiple factors influencing the visual outcome after anti-vascular endothelial growth factor treatment have necessitated the development of new therapeutic approaches. In this review, we provide an analysis of current management strategies to the treatment of diabetic macular edema
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Firstova, V. V., I. G. Shemyakin, and I. A. Dyatlov. "Current understanding of Bacillus anthracis toxin molecules organization and approaches for blocking their cytotoxic action." Russian Journal of Infection and Immunity 9, no. 5-6 (February 1, 2020): 639–47. http://dx.doi.org/10.15789/2220-7619-2019-5-6-639-647.
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Here, we review the data on mechanisms inhibiting cytotoxic effect of anthrax toxin on the immune system cells. Various disease forms, immunopathogenesis and contemporary methods for anthrax treatment are discussed. In addition, an anthrax toxin was outlined, whereas structural and functional organization of the protective antigen, lethal and edema factors was detailed. A mechanism for association of a protective antigen and lethal factor, protective antigen and edema factor leading to formation of a lethal toxin and edema toxin, respectively, was described. Participation of protective antigen domains in the process of interaction with surface receptors of imunocompetent cells as well as features of binding a protective antigen with lethal factor and edema factor are discussed. A mechanism of endosomal toxin complex internalization and subsequent transfer of effector molecules to the cytosol are described. Effects of the lethal factor and the edema factor on components of eukaryotic cells as well as cytotoxicity mechanisms are analyzed. The approaches to block anthrax toxin action at various stages of toxicoemia have been analyzed based on previously uncovered sequential signs of cytotoxic activity for Bacillus anthracis toxins. Currently available chimeric and humanized monoclonal antibodies are capable of neutralizing B. anthracis toxins at diverse assembly stages, particularly considering the drugs inhibiting: inter-receptor interaction between protective antigen with eukaryotic cells; furin-like enzymes activating prepore assembly; protective antigen oligomerization; binding of the lethal factor or edema factor to the protective antigen; translocation of the lethal factor or the edema factor into cell cytosol; transport of protective antigen with lethal factor or edema factor from endosomes; enzymatic activity of lethal factor or edematous factor. The anti-toxin agents approved for anthrax prevention and treatment in Russia and worldwide are discussed. The limitations of anti-toxin agents and perspectives for their improvement are also described including inhibition of lethal factor activity, interference with integration of toxin components, blockade of interactions between toxic complexes and immune cell receptors.
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Brunelle, Cheryl L., Meyha N. Swaroop, Melissa N. Skolny, Maria S. Asdourian, Hoda E. Sayegh, and Alphonse G. Taghian. "Hand Edema in Patients at Risk of Breast Cancer–Related Lymphedema: Health Professionals Should Take Notice." Physical Therapy 98, no. 6 (January 18, 2018): 510–17. http://dx.doi.org/10.1093/ptj/pzy007.
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Abstract Background There is little research on hand edema in the population at risk for breast cancer–related lymphedema (BCRL). Objectives Study aims included reporting potential importance of hand edema (HE) as a risk factor for progression of edema in patients treated for breast cancer at risk for BCRL, reporting risk factors for BCRL, and reporting treatment of HE. Design/Methods This was a retrospective analysis of 9 patients treated for breast cancer in Massachusetts General Hospital's lymphedema screening program who presented with isolated HE. Limb volumes via perometry, BCRL risk factors, and HE treatment are reported. Results Edema was mostly isolated to the hand. Three patients had arm edema >5% on perometry; and 2 of these had edema outside the hand on clinical examination. Patients were at high risk of BCRL with an average of 2.9/5 known risk factors. Arm edema progressed to >10% in 2 high-risk patients. Treatment resulted in an average hand volume reduction of 10.2% via perometry and improvement upon clinical examination. Limitations The small sample size and lack of validated measures of subjective data were limitations. Conclusions In this cohort, patients with HE carried significant risk factors for BCRL. Two out of 9 (22%), both carrying ≥4/5 risk factors, progressed to edema >10%. Isolated HE may be a prognostic factor for edema progression in patients treated for breast cancer at risk for BCRL. Further research is warranted.
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Berthiaume, Yves. "Tumor Necrosis Factor and Lung Edema Clearance." American Journal of Respiratory and Critical Care Medicine 168, no. 9 (November 2003): 1022–23. http://dx.doi.org/10.1164/rccm.2308003.
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Jiao, Guan-Sheng, Seongjin Kim, Mahtab Moayeri, April Thai, Lynne Cregar-Hernandez, Linda McKasson, Sean O'Malley, Stephen H. Leppla, and Alan T. Johnson. "Small molecule inhibitors of anthrax edema factor." Bioorganic & Medicinal Chemistry Letters 28, no. 2 (January 2018): 134–39. http://dx.doi.org/10.1016/j.bmcl.2017.11.040.
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Leysath, Clinton E., Kuang-Hua Chen, Mahtab Moayeri, Devorah Crown, Rasem Fattah, Zhaochun Chen, Suman R. Das, Robert H. Purcell, and Stephen H. Leppla. "Mouse Monoclonal Antibodies to Anthrax Edema Factor Protect against Infection." Infection and Immunity 79, no. 11 (September 12, 2011): 4609–16. http://dx.doi.org/10.1128/iai.05314-11.
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ABSTRACTBacillus anthracisis the causative agent of anthrax, and the tripartite anthrax toxin is an essential element of its pathogenesis. Edema factor (EF), a potent adenylyl cyclase, is one of the toxin components. In this work, anti-EF monoclonal antibodies (MAb) were produced following immunization of mice, and four of the antibodies were fully characterized. MAb 3F2 has an affinity of 388 pM, was most effective for EF detection, and appears to be the first antibody reported to neutralize EF by binding to the catalytic CBdomain. MAb 7F10 shows potent neutralization of edema toxin activityin vitroandin vivo; it targets the N-terminal protective antigen binding domain. The four MAb react with three different domains of edema factor, and all were able to detect purified edema factor in Western blot analysis. None of the four MAb cross-reacted with the lethal factor toxin component. Three of the four MAb protected mice in both a systemic edema toxin challenge model and a subcutaneous spore-induced foreleg edema model. A combination of three of the MAb also significantly delayed the time to death in a third subcutaneous spore challenge model. This appears to be the first direct evidence that monoclonal antibody-mediated neutralization of EF alone is sufficient to delay anthrax disease progression.
Dissertations / Theses on the topic "Edema factor"
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Mohammed, Hesham Hamada Taha. "Molecular analysis of adenylyl cyclase : bacillus anthracis edema factor exotoxin." kostenfrei, 2009. http://www.opus-bayern.de/uni-regensburg/volltexte/2010/1411/.
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Bhandari, Sanjeeb. "Real-world Treatment Outcomes for Diabetic Macular Edema." Thesis, University of Sydney, 2020. https://hdl.handle.net/2123/24071.
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Background Diabetic macular edema (DME) impairs vision and reduces the quality of life. Clinical trials of intravitreal vascular endothelial growth factor (VEGF) inhibitors and steroids for DME have reported remarkable improvements in visual acuity (VA) that had not been previously achieved with laser treatment. Aims This research was divided into three components with a common theme of evaluating real-world treatment outcomes of DME. The first component aimed to study the changes in the treatment patterns for DME in routine clinical practice from 2009 – 2019 and 5-year outcomes. The second component aimed to assess the outcomes of cataract surgery in eyes receiving intravitreal treatments for DME in routine clinical practice. The third aimed to compare the 12-month treatment outcomes of aflibercept with ranibizumab in eyes with DME. Methods These were retrospective analyses of data from a prospectively designed web-based outcomes registry – the Fight Retinal Blindness! Registry. The registry has implemented the DME module to collect data on eyes receiving intravitreal treatment for DME in routine clinical practice. Results Treatment choice changed to predominantly VEGF inhibitors from 2011 onwards. The choice of VEGF inhibitor changed from mainly off-label (bevacizumab) to mainly on-label (ranibizumab or aflibercept). The mean VA at baseline improved from 2009 to 2014 (58 and 68 letters) as did the mean VA change at 5 years (+4.5 and +5.3 letters). Eyes received fewer treatments than those in clinical trials throughout the period studied. The mean VA 6 months after cataract surgery improved and was similar to their matched phakic controls. The mean central subfield thickness (CST) both 6 months before (341μm) and after (360μm) surgery were similar (p=0.08). However, eyes which underwent cataract surgery had thicker maculae and received more injections than their matched controls both before and after surgery. Eyes receiving aflibercept or ranibizumab had improved vision and reduced macular thickness at 12 months when the 2 drugs were compared head to head for DME. Eyes receiving aflibercept had greater reduction in CST than those receiving ranibizumab. Among eyes with initial VA ≤ 20/50, larger VA gains were observed in eyes treated with aflibercept. Conclusions VEGF inhibitors became the preferred treatment for DME in real-world setting during the period studied, although they were given less often than in the pivotal clinical trials. Visual outcomes of cataract surgery in eyes with DME treatment were acceptable. Aflibercept outcomes were somewhat better than ranibizumab over the first 12 months of DME treatment. These findings may be a useful guide to clinicians as to the optimal management of eyes with DME.
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Gómez, Sánchez Sandra. "Influencia de la interfase vitreorretiniana en la evolución del edema macular diabético después del tratamiento con inyecciones intravítreas de inhibidores del factor de crecimiento endotelial vascular." Doctoral thesis, Universitat Autònoma de Barcelona, 2017. http://hdl.handle.net/10803/456317.
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JUSTIFICACIÓN: Uno de los tratamientos de primera línea del edema macular diabético
(EMD) son las inyecciones intravítreas de fármacos inhibidores del factor de crecimiento
endotelial vascular (antiVEGF). El alto impacto clínico, social y económico de esta
patología ha hecho aumentar el interés en la detección de biomarcadores pronósticos
de respuesta al tratamiento con el fin de mejorar la individualización del tratamiento
disminuyendo la sobrecarga asistencial en los departamentos de oftalmología. El
desprendimiento de vítreo (DVP) en pacientes diagnosticados de EMD es un
acontecimiento poco estudiado, sin embargo, los estudios publicados coinciden en una
menor tasa de DVP en pacientes con EMD que en pacientes sin EMD.
OBJETIVOS: Demostrar que las inyecciones intravítreas de antiVEGF en pacientes con
EMD inducen el DVP, demostrar que la presencia de DVP en pacientes con EMD mejora
la eficacia del tratamiento con inyecciones de antivEGF, y demostrar que la presencia de
DVP disminuye el número de inyecciones de antiVEGF necesarias para el tratamiento
del EMD.
MATERIAL Y MÉTODOS: Se ha realizado un estudio observacional, prospectivo y
longitudinal, comparando dos grupos en función de la presencia (Grupo 1: 18 ojos) o
ausencia (Grupo 2: 20 ojos) de adherencia vitreomacular (AVM) a los 12 meses de
seguimiento. El protocolo de estudio consistía en visitas cada 2 meses durante 1 año,
evaluando en todas las visitas la agudeza visual (AV), el grosor foveal (CFT) y el grado de
DVP. El régimen de tratamiento consistió en una pauta fija de 3 inyecciones intravítreas
de Ranibizumab cada 2 meses y después una pauta pro re nata bimestral. Se incluyó
también un grupo control de 10 ojos de pacientes diabéticos sin EMD para analizar la
incidencia de DVP al año de seguimiento.
RESULTADOS: Al inicio, un 76.32% de los pacientes presentaban AVM, y al año se
observó una tasa de acontecimiento del DVP del 37.9% en pacientes que habían recibido
tratamiento con inyecciones intravítreas de antiVEGF mientras que no se observó
ningún caso en el grupo control (p<0.001). La mejoría de AV fue de 6.94 letras en el
Grupo 1 (p=0.03) y de 4.9 letras en el Grupo 2 (p=0.08), siendo esta diferencia no
estadísticamente significativa (p=1.00). La reducción del CFT fue de 259±239.62μm en
el Grupo 1 (p=0.0002) y de 118±148.33μm en el Grupo 2 (p=0.003), siendo esta
diferencia no estadísticamente significativa (p=0.06). Los pacientes del Grupo 1
recibieron una media de 4.83±1.79 inyecciones de antiVEGF, y los del Grupo 2, 5.4±1.76
inyecciones, siendo esta diferencia no estadísticamente significativa (p=0.332).
CONCLUSIONES: Las inyecciones intravítreas repetidas de antiVEGF en pacientes con
EMD inducen el DVP en un 37.9% de los casos con AVM. La presencia de DVP no mejora
la eficacia del tratamiento con antiVEGF, al contrario, encontramos una tendencia a una
mayor reducción del CFT en pacientes con AVM. Los pacientes con EMD y DVP no
requieren menos inyecciones de antiVEGF durante un año.RATIONALE: One of the first-line treatments of diabetic macular edema (DME) are intravitreal injections of vascular endothelial growth factor inhibitor (antiVEGF) drugs. The high clinical, social and economic impact of this pathology has increased interest in the detection of prognostic biomarkers of response to treatment in order to improve the individualization of treatment, reducing the burden of care in ophthalmology departments. Posterior vitreous detachment (PVD) in patients diagnosed with DME is a poorly studied event, however, published studies agree on a lower rate of DVP in patients with DME than in patients without DME. OBJECTIVES: To demonstrate that intravitreal injections of antiVEGF drugs in patients with DME induce PVD, to demonstrate that the presence of PVD in patients with DME improves the efficacy of antivEGF injection therapy, and to demonstrate that the presence of PVD reduces the number of injections of Anti-VEGF necessary DME treatment. MATERIAL AND METHODS: An observational, prospective and longitudinal study was performed comparing two groups based on presence (Group 1: 18 eyes) or absence (Group 2: 20 eyes) of vitreomacular adhesion (VMA) at 12 months follow-up. The study protocol consisted of visits every 2 months for 1 year, evaluating visual acuity (VA), foveal thickness (CFT) and PVD grade in each visit. The treatment regimen consisted of a fixed regimen of 3 intravitreal injections of Ranibizumab every 2 months, followed by a bimonthly pro re nata regimen. We also included a control group of 10 eyes of diabetic patients without EMD to analyze the incidence of PVD at one year of follow-up. RESULTS: At baseline, 76.32% of the patients had VMA, and at month twelve, a PVD event rate of 37.9% was observed in patients who had received intravitreal injections of antiVEGF while no cases were seen in the control group (P <0.001). The VA improvement was 6.94 letters in Group 1 (p=0.03) and 4.9 letters in Group 2 (p=0.08), this difference being not statistically significant (p = 1.00). CFT reduction was 259±239.62μm in Group 1 (p = 0.0002) and 118±148.33μm in Group 2 (p = 0.003), this difference being not statistically significant (p = 0.06). Patients in Group 1 received an average of 4,83±1,79 injections of anti-VEGF, and those in Group 2, 5.4±1.76 injections, this difference being not statistically significant (p=0.332). CONCLUSIONS: Repeated intravitreal injections of antiVEGF in patients with DME induce PVD in 37.9% of cases with VMA. The presence of PVD does not improve the efficacy of antiVEGF treatment; on the contrary, we found a tendency towards a greater reduction of CFT in patients with VMA. Patients with DME and PVD do not require fewer injections of anti-VEGF for one year.
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Berk, Benjamin-Andreas. "Brain-derived neurotrophic factor-induzierte neuroprotektive Osmoregulation der Müller-Gliazelle der Rattenretina." Doctoral thesis, Universitätsbibliothek Leipzig, 2015. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-170385.
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Einleitung: Die Ausbildung eines Netzhautödems ist eine Hauptursache für die Verschlechterung des Sehvermögens bei ischämisch-hypoxischen und inflammatorischen Netzhauterkrankungen. Neben der erhöhten Permeabilität der Blut-Retina-Schranke trägt eine Wasserakkumulation in Netzhautzellen zur Ausbildung eines Netzhautödems bei. Müllerzellen regulieren die retinale Ionen- und Osmohomöostase, indem sie einen transzellulären Ionen- und Wassertransport vermitteln. Zudem kontrollieren Müllerzellen die Größe des Extrazellularraumes, indem sie bei neuronaler Aktivität eine Zellkörperschwellung – ausgelöst durch eine Verkleinerung der extrazellulären Osmolarität – verhindern. Unter pathologischen Bedingungen ist die Volumenregulation gestört, sodass Müllerzellen bei Hypoosmolarität anschwellen. Diese Müllerzellschwellung und eine Glutamat-induzierte Schwellung retinaler Neurone tragen zur Ausbildung eines zytotoxischen Netzhautödems bei. Neuroprotektive Faktoren wie BDNF (brain-derived neurotrophic factor) und bFGF (basic fibroblast growth factor) stimulieren das Überleben retinaler Neurone und verzögern so die retinale Degeneration. Zielstellung: Es war zu zu ermitteln, ob BDNF die zytotoxische Schwellung von Müller- und Bipolarzellen der Rattennetzhaut verhindert. Material und Methoden: Es wurden Netzhautschnitte und isolierte Müller- und Bipolarzellen von 55 adulten Long-Evans-Ratten (durchschnittlich 8-15 Zellen pro Versuchsreihe) verwendet. Eine osmotische Schwellung von Müller- und Bipolarzellen wurde durch eine Superfusion der Schnitte oder der Zellen mit einer 60%igen hypoosmolaren Lösung in Ab- oder Anwesenheit von Bariumchlorid induziert. Die maximale Querschnittsfläche von Müller- und Bipolarzellsomata wurde vor und nach einer vierminütigen Superfusion mit einem konfokalen Laserscanningmikroskop aufgezeichnet. Die nach der Superfusion ermittelte Querschnittsfläche wurde zu den anfänglich gemittelten Kontrollwerten in Beziehung gesetzt und prozentual als Mittelwert mit Standardfehler bestimmt. Mit Hilfe des Prism-Statistikprogramms (Graphpad) wurden die Ergebnisse mittels einem one-way ANOVA Test und einem nachfolgenden Bonferroni\'s multiple comparison Test sowie durch einen Mann-Whitney U Test statistisch analysiert. Ergebnisse: Bei Anwesenheit von BDNF wurde die osmotische Schwellung von Müllerzellen konzentrationsabhängig sowohl in Netzhautschnitten als auch in isolierten Zellen inhibiert. Ebenso inhibierte BDNF konzentrationsabhängig die Schwellung von Bipolarzellen in Netzhautschnitten, jedoch nicht in isolierten Zellen. In Schnitten von postischämischen Netzhäuten bewirkte BDNF eine Schwellungsinhibition von Müllerzellen, nicht aber von Bipolarzellen. Mit pharmakologischen Blockern wurde die durch BDNF induzierte Signalkaskade untersucht. Die BDNF-Schwellungsinhibition von Müllerzellen wurde durch eine Aktivierung von TrkB bewirkt. Die TrkB-Aktivierung führte in Müllerzellen zu einer Transaktivierung von FGF-Rezeptoren sowie zu einer Aktivierung einer glutamatergen-purinergen Signalkaskade, von der bekannt ist, dass sie die osmotische Müllerzellschwellung unterdrückt. Da bFGF die osmotische Müllerzellschwellung inhibiert, wird die Transaktivierung der FGF-Rezeptoren wahrscheinlich durch eine BDNF-induzierte Freisetzung von bFGF aus Müllerzellen vermittelt. Die Ergebnisse lassen vermuten, dass BDNF indirekt auf Bipolarzellen wirkt, indem es eine Freisetzung von Faktoren wie bFGF aus Müllerzellen induziert. Schlussfolgerungen: Die Schwellungsinhibition von Müller- und Bipolarzellen könnte ein neuroprotektiver Mechanismus von BDNF in der Netzhaut darstellen. Während BDNF direkt TrkB auf Müllerzellen aktiviert, ist die Inhibition der Bipolarzellschwellung indirekt und durch die Ausschüttung von glialen Faktoren wie bFGF vermittelt. Der Verlust des Effektes von BDNF auf die Bipolarzellschwellung in ischämischen Netzhäuten könnte darauf zurückzuführen sein, dass gliotische Müllerzellen keine glialen Faktoren mehr in Reaktion auf BDNF freisetzen. Der Verlust des glialen Einflusses auf die Bipolarzellvolumenhomöostase könnte zur Neurodegeneration in der ischämischen Netzhaut beitragenIntroduction: Tissue edema is a major blinding complication of ischemic-hypoxic and inflammatory retinal diseases. In addition to the hyperpemeability of the blood-retinal barrier, water accumulation in retinal cells resulting in cellular swelling may contribute to the development of retinal edema. Müller glial cells regulate the retinal ion and water homeostasis by allowing transcellular ion and water fluxes. During neuronal activity Müller cells control the extracellular space volume by autocrine inhibition of cellular swelling caused by the reduction of extracellular osmolarity. However, under pathological conditions, Müller cells are not capable to regulate their volume so that they swell rapidly under hypoosmolarity. The osmotic swelling of Müller glial cells and the glutamate induced swelling of retinal neurons contribute to the development of cytotoxic retinal edema. Various neuroprotective factors including brain-derived neurotrophic factor (BDNF) and basic fibroblast growth factor (bFGF) stimulate the survival of retinal neurons and thus delay the retinal degeneration. Objective: The objective of the study is to determine whether BDNF inhibits the osmotic swelling of Müller and bipolar cells of the rat retina. Material and Methods: Retinal slices and freshly isolated Müller and bipolar cells of 55 adult Long-Evans rats (in average 8-15 cells per trial) were used. Osmotic swelling of Müller and bipolar cells was induced by superfusion of retinal slices or isolated cells with a 60% hypoosmotic extracellular solution in the absence or presence of barium chloride. The maximal cross-sectional area of Müller and bipolar cell somata was recorded before and after a four minute-long superfusion by using a laser scanning microscope. To determine the extent of cell soma swelling, the cross-sectional area of the cell body extent after superfusion was related to the former averaged cross-sectional area. Results were given as means with standard error as percent values. Statistical analysis was made with Prism (Graphpad) and the significance was determined by the One-way ANOVA test followed by Bonferroni\'s multiple comparison test and the Mann-Whitney U test, respectively. Results: We found that BDNF inhibits dose-depending the osmotic swelling of Müller cells in retinal slices and of isolated cells. BDNF also inhibited dose-depending the osmotic swelling of bipolar cells in retinal slices; however, it did not inhibit the osmotic swelling in isolated bipolar cells. In slices of postischemic retinas, BDNF inhibited the swelling of Müller cells but not the swelling of bipolar cells. The BDNF induced signal transduction cascade was examined by simultaneous administration of blocking agents with the receptor agonists in the hypoosmotic solution. The BDNF-induced inhibition of the osmotic Müller cell swelling was mediated by activation of TrkB. Activation of TrkB in Müller cells results in transactivation of FGF receptors and in an activation of a glutamatergic-purinergic signal transduction cascade which is known to inhibit the osmotic swelling of the cells. Since bFGF also inhibits the osmotic swelling of Müller cells, it can be assumed that the transactivation of FGF receptors is mediated by a BDNF-induced release of bFGF from Müller cells. The results suggest that the effect of BDNF on bipolar cells is indirect by inducing a subsequent release of glial factor from Müller cells such as bFGF. Conclusion: The results show that BDNF inhibits the osmotic swelling of Müller and bipolar cells. The inhibition of cytotoxic cell swelling may contribute to the neuroprotective action of BDNF in the retina. While BDNF acts directly in Müller cells, the BDNF-induced inhibition of the bipolar cell swelling is indirect and mediated by the release of glial factors such as bFGF from Müller cells. The abrogation of the BDNF-induced inhibition of the osmotic bipolar cell swelling in the postischemic retina could be explained with the impairment of the release of glial factors by Müller cells. The abrogation of the Müller cell-mediated regulation of the bipolar cell volume could contribute to the neuronal degeneration in the ischemic retina
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RASSI, Alan Ricardo. "Estudo das alterações retinianas em olhos de coelhos após injeções intravítreas seriadas de infliximabe." Universidade Federal de Goiás, 2011. http://repositorio.bc.ufg.br/tede/handle/tde/1523.
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Previous issue date: 2011-10-08The objective of this study was to determine the levels of toxicity of two and three intravitreous injections of infliximab to the retina and choroid of albino rabbits by means of histological, electroretinographic and clinical ophthalmological tests. Twelve New Zealand albino rabbits (24 eyes) were used in the study. Each eye was given two (n=10) or three (n=10) serial intravitreous 2 mg injections of infliximab dissolved in 0.06 ml of saline, at monthly intervals. A separate group of rabbits (n=4 eyes) served as a control group. Ninety days after the first injection, the rabbits underwent electroretinographic and clinical ophthalmological tests. After being enucleated, the eyes underwent histological examination. No clinical ophthalmologic abnormalities were detected in the 24 eyes studied. The histological change noted was the presence of rare lymphocytes and eosinophiles in the posterior vitreous of four eyes subjected to two injections and six eyes subjected to three injections of infliximab, but it was not considered clinically significant. One clinically significant abnormality was found, a severe inflammatory reaction with vitreous exudates and ganglion cell edema in both eyes of a single rabbit, subjected to two to three injections of infliximab. The electroretinographic tests showed amplitudes that were on the average 12% smaller than those obtained before the treatment. However, there were no statistically significant differences when comparing amplitude or the implicit time between the pre and post-treatment electroretinographic findings, in all groups examined. Then, two and three intravitreous 2 mg injections of infliximab in eyes of rabbits at monthly intervals did not cause any changes after a 90-day follow-up, according to histological, electroretinographic tests and clinical ophthalmological evaluation. It was concluded that serial intravitreous infliximab doses to rabbits is a safe procedure.
O objetivo deste trabalho foi determinar os níveis de toxicidade de duas e três aplicações intravítreas de infliximabe na retina e coroide de coelhos albinos, por meio de exames clínicos oftalmológicos, eletrorretinográficos e histológicos. Foram utilizados doze coelhos albinos (24 olhos) da raça New Zealand. Cada olho recebeu duas (n=10 olhos) ou três (n=10 olhos) injeções intravítreas seriadas de 2 mg de infliximabe dissolvidos em 0,06 ml de solução salina, em intervalos mensais. Um grupo separado de olhos (n=4 olhos) serviu como controle. Noventa dias após a primeira injeção, os coelhos foram novamente submetidos a exames clínicos oftalmológicos e eletrorretinográfico e, após enucleados, os olhos foram submetidos a exame histológico. Nos 24 olhos estudados, não foram detectadas alterações clínicas oftalmológicas. A alteração histológica notada foi a presença de raros linfócitos e eosinófilos na região posterior do vítreo de quatro olhos submetidos a duas aplicações e de seis olhos que receberam três aplicações de infliximabe, mas sem significado clínico. Foi encontrada uma única alteração clinicamente significante, caracterizada como reação inflamatória grave, com presença de exsudatos vítreos nos dois olhos de um coelho, que foi submetido a duas e três aplicações de infliximabe. Os exames eletrorretinográficos mostraram amplitudes em média 12% menores do que aquelas obtidas antes do tratamento, porém sem diferenças estatisticamente significantes, comparando-se a amplitude ou o tempo implícito entre os achados eletrorretinográficos pré e pós-tratamento em todos os grupos examinados. Assim, duas e três aplicações intravítreas de infliximabe em olhos de coelhos em intervalos mensais, na dosagem de 2 mg, não provocaram alterações após seguimento de noventa dias, quer no exame histológico, na eletrorretinografia ou na avaliação clínica oftalmológica. Conclui-se que doses seriadas de infliximabe por via intravítrea em coelhos é um procedimento seguro.
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Pitard, Irène. "Analyse du mécanisme d'action d'inhibiteurs ciblant l'activation allostérique du facteur œdématogène de Bacillus anthracis." Electronic Thesis or Diss., Sorbonne université, 2020. http://www.theses.fr/2020SORUS420.
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Le facteur œdémateux (EF), une toxine majeure de Bacillus anthracis, est activé par la calmoduline de l’hôte (CaM) pour produire des concentrations supra physiologiques d'AMP cyclique (AMPc) conduisant à une perturbation des voies de signalisation. L'interaction EF-CaM induit des changements conformationnels dans une région switch allostérique de EF conduisant à la formation du site catalytique fonctionnel. Des études antérieures in silico ciblant cette région switch, complétées par des données expérimentales, ont montré que les uréidoacides thiophènes (TUA) inhibent l’activité enzymatique de EF. Cependant, les connaissances sur le site de liaison et sur l'interaction étaient manquantes. Nous présentons ici une étude de l'interaction du TUA-diCl, le composé le plus actif, avec les protéines EF, CaM et le complexe EF-CaM à l'aide d’essais biochimiques couplés à des méthodes biophysiques et de modélisations moléculaires. Le TUA-diCl interagit avec EF isolé, le complexe EF-CaM et de manière inattendue avec CaM. L’étude du site de liaison entre le composé TUA-diCl et la protéine CaM par RMN indique que le composé se lie aux patchs hydrophobes de CaM qui deviennent accessibles lorsque la CaM est complexée par les ions calciums. Ceci entraîne un compactage de la structure de CaM et des changements de la dynamique interne de la protéine. Les données enzymatiques, de fluorescence et de RMN montrent que l'inhibition d'EF est due à l'interaction du composé sur EF et ne dépend pas de la présence de CaM. Des expériences de compétition entre le TUA-diCl et l’inhibiteur du site catalytique EF 2’-MANT-3’-dATP, indiquent que TUA-diCl est un inhibiteur allostérique de EF. Les expériences HDX-MS ont révélé que le TUA-diCl se lierait au domaine hélicoïdal de EF, une région critique pour l'insertion de CaM. De plus, des approches in silico ont mis en évidence plusieurs sites de liaison possible dans le domaine hélicoïdal. Par conséquent, TUA-diCl représente une nouvelle classe d'inhibiteurs de EF avec un mécanisme d'action allostérique et ouvrant la voie vers la conception de molécules thérapeutiques innovantesEdema factor (EF), a major Bacillus anthracis toxin, is activated by host calmodulin (CaM) to produce supraphysiological concentrations of cyclic AMP (cAMP) thus perturbing intracellular signaling. The EF-CaM interaction induces conformational changes in an allosteric switch region of EF that lead to the formation of the catalytic site. Previous in silico studies targeting this switch region, complemented with experimental data, showed that thiophen ureidoacids (TUA) inhibit the enzyme catalytic activity. However, knowledge of the binding site and inhibition mode of TUA compounds are still lacking. Here, we characterize the interaction of the most active TUA compound (TUA-diCl) with EF, CaM and EF-CaM using biochemical assays coupled to biophysical methods and molecular modeling. We show that TUA-diCl interacts with EF, EF-CaM and unexpectedly with CaM. Mapping of the binding site by NMR, showed that TUA-diCl binds to the exposed hydrophobic patches of calcium loaded CaM, causing the compaction and changes in internal dynamics of the protein. Importantly, enzymatic, fluorescence and NMR data show that EF inhibition is due to the interaction of the compound with EF and is CaM-independent. Furthermore, competition experiments between TUA-diCl and the EF catalytic-site inhibitor 2’-MANT-3’-dATP, indicate that TUA-diCl is an allosteric inhibitor of EF. HDX-MS identifies a putative binding site of TUA-diCl on the helical domain of EF, a critical region for CaM insertion. Several possible binding pockets in the helical domain are analyzed in silico. TUA-diCl represents a new class of EF inhibitors with an allosteric mechanism, opening the way towards the design of innovative therapeutic compounds
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Sandra, Jovanović. "Uloga inhibitora vaskularnog endotelnog faktora rasta u terapiji dijabetičnog makularnog edema." Phd thesis, Univerzitet u Novom Sadu, Medicinski fakultet u Novom Sadu, 2015. http://www.cris.uns.ac.rs/record.jsf?recordId=91828&source=NDLTD&language=en.
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Dijabetesna retinopatija je među vodećim uzročnicima stečenog slepila, kako u razvijenim zemljama, tako i zemljama u razvoju. Dijabetesna retinopatija je jedna odnajčešćih komplikacija Dijabetes Mellitus-a. U sklopu dijabetesne retinopatije jedan od najranijih razloga koji dovodi do pada vidne oštrine je dijabetični makularni edem (DME). Pad vidne oštrine kod pacijenata sa dijabetesom narušava njihov kvalitet života i umanjuje radnu sposobnost. Dosadašnji oblik lečenja laserfotokoaguacijom makule, nije dao zadovoljavajuće rezultate. U novije vreme sve više je zastupljeno farmakološko lečenje edema koje podrazumeva intrvitrealnu aplikaciju lekova iz grupe inhibitora vaskularnog endotelnog faktora rasta (VEGF inhibitori), koji dovodi do stabilizacije zidova krvnih sudova. Cilj ove studije je da se ispita efikasnost lečenja DME uz pomoć intravitrealno aplikovanih lekova iz grupe inhibitora vaskularnog endotelnog faktora rasta u odnosu na konvencionalno do sada priznato lečenje laserfotokogulacijom makule. Efikasnost lečenja je procenjivana na dva načina: anatomski, na osnovu smanjenja centralne makularne debljine izražene u μm, merene metodom optičke koherentne tomografije, i funkcionalno, na osnovu poboljšanja vidne oštrine koja je izražavana u log MAR jedinicama. U ovoj prospektivnoj, randomiziranoj kliničkoj studiji sa minimumom praćenja od 6 meseci, u eksperimentalnoj grupi tretiran je 51 pacijent,odnosno 84 oka aplikacijom bevacizumaba (anti VEGF agens) u dozi od 1,25 mg, sa ili bez dodatnog laser tretmana. Uz prosečno 2,46 inekcije postignuta je prosečna redukcija centralne makularne debljine od 139,15 μm. Dobijene vrednosti su nakon svake aplikovane doze su značajno bolje u odnosu na početnu. Edemi sa većom centralnom makularnom debljinom su zahtevali tretman sa većim brojem inekcija. Kod većih edema je postignuta i veća redukcija centralne makularne debljine. U odnosu na vidnu oštrinu u eksperimentalnoj grupi postignuto je poboljšanje od 0,135 log MAR jedinica. Efekat lasera kao samostalne terapije u kontrolnoj grupi (50 pacijenata, 92 oka) nije bioznačajan ni u pogledu smanjenja centralne makularne debljine kao ni na osnovu poboljšnja vidne oštrine. Tretman bevacizumabom samostalno ili u kombinaciji sa laserom je efikasniji u tretmanu DME u odnosu na konvencionalni tretman laserfotokoaguacijom koji potvrđeno dovodi do stabilizacije stanja. Značaj ove studije je potvrda efikasnosti i bezbednosti jednog novog oblika lečenja koji samostalno ili u kombinaciji sa laser tretmanom predstavlja novi protokol lečenja dijabetičnog makularnog edema.Diabetic retinopathy is among the leading causes of acquired blindness in developed countries, as well as in developing countries. Diabetic retinopathy is one of the most frequent Diabetes Mellitus complications. Within diabetic retinopathy, diabetic macular edema (DME) is one of the earliest causes of the loss of visual acuity. Impaired vision causes decline in life quality in diabetic patients and it decreases theirworking ability. Up to this date, laser photocoagulation treatment has not givensatisfactory results. Recently, new promising treatment forms have emerged, including the intravitreal application of vascular endothelium growth factor (VEGF inhibitors), which lead to stabilization of the vessel wall. The aim of this study is to evaluate the efficacy of DME treatment consisting of intravitreal VEGF inhibitor application alone or as a part of combined treatment (intravitreal VEGF inhibitor plus laser photocoagulation) compared with conventional laser treatment alone. The effect of treatment was evaluated according to morphological parameters by measuring central macular thickness (CMT) in μm with optical coherence tomography, and according to functional parameter by visual acuity in log MAR scale. In this prospective randomized clinical trial, with minimum follow up of 6 months, in experimental group 51 patient, or 84 eyes were treated with bevacizumab (VEGF inhibitor) in 1.25 mg dosage, alone or in combination with laser. The mean reduction in was 139.15 μm, which was achieved with 2.46 doses on average. The difference between the final and initial CMT values after each dos age was tatistically significant.Edemas with high central macular thickness required high number of intravitealaplicatons and the reduction was higher. In our study, mean visual acuity improved significantly in 0.135 log MAR. In control group (50 patient, 92 eyes) treated with laserphotocolagulation alone, the effect on visual acuity and central acular thickness was not statistically significant. The treatment with bevacizumab alone or in combinedtreatment is more effective in treating DME than conventional macular laser treatment alone, from both - anatomical and functional perspective. The importance of this study is confirmation of the efficacy and safety of a new form of treatment and the introduction of a new protocol for the treatment of diabetic macular edema.
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McCafferty, Sean, April Harris, Corin Kew, Tala Kassm, Lisa Lane, Jason Levine, and Meisha Raven. "Pseudophakic cystoid macular edema prevention and risk factors; prospective study with adjunctive once daily topical nepafenac 0.3% versus placebo." BIOMED CENTRAL LTD, 2017. http://hdl.handle.net/10150/623120.
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Background: Define the effectiveness of a topical non-steroidal anti-inflammatory drug (NSAID) added to topical steroid use after uncomplicated phacoemulsification for the prevention of pseudophakic cystoid macular edema (PCME) using a prospective, randomized, double-masked, placebo-controlled clinical study. Methods: Eyes (1000) were randomized to placebo (497) or nepafenac 0.3% (503) used once daily, post-operatively for 5 weeks at two ophthalmology clinics. Diagnosis of PCME was made by clinical, ocular coherence tomography (OCT), and with fluorescein angiography confirmation. Correlation of PCME to NSAID use and the presence of pre-operative risk factors for PCME were assessed including, contralateral PCME, diabetic retinopathy, retinal vein occlusion, macular hole, epiretinal membrane, macular degeneration, retinal detachment repair, and prostaglandin use. Results: PCME was the most common complication associated with routine cataract surgery (4.2% with PCME risk factors, 2.0% with risk factors excluded). Topical nepafenac 0.3% significantly reduces the incidence of PCME compared to placebo when used after routine cataract surgery (p = .0001). When patients with pre-operative risk factors are excluded, the incidence of PCME between treatment and placebo groups is equivalent (p = 0.31). PCME relative risk (RR) was most significant in contralateral PCME (RR 19.5), diabetic retinopathy (RR 13.1), retinal vein occlusion (RR 12.9), macular hole (RR 7.7), and epiretinal membrane (RR 5.7). Prostaglandin use and previous retinal detachment were not shown to increase risk. Conclusion: Pseudophakic cystoid macular edema is common after phacoemulsification cataract surgery. Topical nepafenac 0.3% reduces PCME in patients with pre-operative risk factors for PCME compared to placebo but shows no benefit in patients without pre-operative risk factors.
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Rud, Nicole Ann. "Environmental factors influencing the physiological disorders of edema on ivy geranium (Pelargonium peltatum) and intumescences on tomato (Solanum lycopersicum)." Thesis, Manhattan, Kan. : Kansas State University, 2009. http://hdl.handle.net/2097/2380.
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Figueras, Roca Marc. "Caracterització dels Factors Clínics i Biològics Associats a l’Edema Macular Diabètic en la Diabetis Mellitus Tipus II." Doctoral thesis, Universitat de Barcelona, 2018. http://hdl.handle.net/10803/663845.
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INTRODUCCIÓ:
L'edema macular diabètic (EMD) és una complicació clínica associada a la retinopatia diabètica (RD) i és la primera causa de pèrdua visual en diabètics en el món desenvolupat. Implica l'extravasació de fluids i lípids en l'àrea macular, la regió de la retina responsable de la visió central. Alguns dels seus factors de risc, com la hiperglucèmia crònica, són comuns amb la RD. Tanmateix, altres agents claus en la seva etiopatogènia, com els mediadors moleculars de la inflamació i diferents factors de creixement, no han estat estudiats en profunditat, especialment en relació amb la seva presència diferencial lligada a l'existència d'EMD.
OBJECTIU:
Estudiar l'associació entre factors metabòlics i inflamatoris en sang perifèrica i la presència d'EMD així com la seva associació a certes característiques intraoculars.
MATERIALS I MÈTODE:
Es planteja un estudi observacional de tall transversal sobre pacients diabètics amb RD en dos grups, aquells amb EMD associat (n=58) i aquells sense EMD (n=18). Es va realitzar un estudi detallat de la presentació oftalmològica en aquests grups d'acord als criteris d'inclusió i exclusió establerts, incloent diferents paràmetres qualitatius i quantitatius de tomografia de coherència òptica macular (OCT) a tots els pacients i angiografia fluoresceínica retinal de camp ampli (AFCA) en els casos d'EMD. A més a més, es va dur a terme un estudi complet de factors metabòlics (glicèmia, creatinina, colesterol total, LDL colesterol, HDL colesterol, triglicèrids, enzims hepàtics, hemoglobina i hemoglobina glicada) mitjançant anàlisi sanguínia així com de mediadors inflamatoris sèrics (citocines, quimiocines i factors de creixement), també en tots els pacients. El panell de mediadors inflamatoris estudiat, d'acord al coneixement previ disponible tant en mostres sanguínies com intraoculars, inclogué: IL-1β, IL-3, IL-6, IL-8, IL-10, MCP-1, IP-10, IFN-γ, TNF-α i VEGF.
RESULTATS:
Els paràmetres metabòlics i inflamatoris sèrics estudiats no s'han associat directament a la presència d'EMD. Tanmateix, quan aquesta complicació intraocular està present, certes característiques de la mateixa s'associen de forma estadísticament significativa a determinats mediadors sistèmics: la presència d'engruiximent difús de la retina per OCT es relaciona amb majors xifres sèriques d'IL-6; l'existència d'edema macular quístic per OCT s'associa a menors nivells en sang perifèrica d'IL-10; i, finalment, s'han objectivat majors xifres sèriques d'IL-8 i VEGF en aquells casos amb augment de la zona avascular foveal mesurada per AFCA.
CONCLUSIÓ:
El desenvolupament d'EMD no s'associa aparentment a patrons diferenciats de mediadors inflamatoris o metabòlics pel que fa a sang perifèrica. Tanmateix, certes característiques anatòmiques de l'EMD sí que es relacionen amb determinades molècules en l'àmbit sistèmic. Tot i el seu caràcter pilot, aquests resultats aporten valuosa informació sobre les que proposar estratègies futures en el maneig individualitzat del pacient amb EMD.INTRODUCTION: Diabetic macular edema (DME) represents a clinical complication of diabetic retinopathy (DR) and is the major cause of vision loss in diabetic patients in the developed world. It implies fluid and lipid extravasation in the macular area of the retina, which is accountable of main visual acuity. Several DME risk factors, as chronic hyperglycemia, are common to DR. However, other etiopathogenic agents such as inflammatory molecules and growth factors have not been widely studied, specially regarding its differential association to DME. AIMS: To study the association between peripheral blood metabolic and inflammatory factors and presence of diabetic macular edema (DME) and its related anatomic features in type 2 diabetic mellitus (T2DM) patients. MATERIAL AND METHODS: Observational cross-sectional study on a proof of concept basis. Seventy-six T2DM included patients were divided based on the presence (n = 58) or absence of DME (n = 18) according to optical coherence tomography (OCT). Ultra-widefield fluorescein angiography (UWFA) was performed in DME patients. Fasting peripheral blood sample testing included glycemia, glycated hemoglobin, creatinin and lipid levels among others. Serum levels of a broad panel of cytokines and inflammatory mediators were also analyzed. OCT findings included central subfoveal thickness, diffuse retinal thickness (DRT), cystoid macular edema (CME), serous retinal detachment and epirretinal membrane. UWFA items included pattern of DME, presence of peripheral retinal ischemia and enlarged foveal avascular zone (FAZ). RESULTS: Metabolic and inflammatory factors did not statistically differ between groups. However, several inflammatory mediators did associate to certain ocular items of DME cases: IL-6 was significantly higher in patients with DRT (p = 0.044), IL-10 was decreased in patients with CME (p = 0.012), and higher IL-8 (p = 0.031) and VEGF levels (p = 0.031) were observed in patients with enlarged FAZ. CONCLUSION: Inflammatory and metabolic peripheral blood factors in T2DM may not be differentially associated to DME when compared to non-DME cases. However, some OCT and UWFA features of DME such as DRT, CME and enlarged FAZ may be associated to certain systemic inflammatory mediators.
Books on the topic "Edema factor"
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Davison, Earl. Macular Edema: Risk Factors, Treatment Options and Long-Term Outcomes. Nova Science Publishers, Incorporated, 2014.
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Loochtan, Aaron I., Jodi Dodds, and Cheryl D. Bushnell. Hemorrhagic Stroke Management in Pregnancy. Edited by Emma Ciafaloni, Cheryl Bushnell, and Loralei L. Thornburg. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190667351.003.0015.
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Intracerebral hemorrhage (ICH) during pregnancy and the puerperuim is a rare but potentially devastating complication of pregnancy. It is a condition that requires emergent medical attention and inclusion of multiple medical and or surgical specialists. Accurate diagnosis based on clinical exam and supported by neuroimaging techniques is essential. Medical management is the mainstay in most cases including post-hemorrhage blood product consideration, reversal agents if on anti-coagulation, blood pressure control, cerebral edema management, and treatment of seizures. Circumstances also arise in which surgical intervention is needed. It is important to also discuss optimal timing of delivery. Postpartum care including close blood pressure control, deep vein thrombosis prophylaxis (DVT), and risk factor modification are important. Ethical situations sometimes arise and must also be considered with respect to the mother and child.
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Baijal, Rahul, and Carlos J. Campos. Diabetic Ketoacidosis in a Child with Acute Surgical Abdomen. Edited by Erin S. Williams, Olutoyin A. Olutoye, Catherine P. Seipel, and Titilopemi A. O. Aina. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190678333.003.0040.
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Management of the pediatric surgical patient in diabetic ketoacidosis (DKA) is particularly challenging given the electrolyte and acid-base abnormalities, compounded with the risk of cerebral edema. This chapter highlights the risk factors, diagnosis, and treatment plan, for the pediatric surgical patient who presents in DKA. This chapter will help the reader identify children at risk for DKA, understand the clinical presentation and pathophysiology of DKA, identify children at risk for cerebral edema, manage cerebral edema in children with DKA, manage DKA in children, and understand the anesthetic implications in children with DKA.
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Gore, Cheryl, Junzheng Wu, and C. Dean Kurth. Stridor after Extubation. Edited by Erin S. Williams, Olutoyin A. Olutoye, Catherine P. Seipel, and Titilopemi A. O. Aina. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190678333.003.0066.
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Postextubation stridor arises from glottic and subglottic edema caused by ischemia of the tracheal mucosa from pressure by the endotracheal tube. Multiple risk factors have been described; preventive measures include appropriate tube sizing, air leak tests, administration of steroids, and smooth airway management techniques, such as atraumatic intubation. When stridor does occur, cool humidified air as well as racemic epinephrine may be used as treatment. The patient is safe for discharge once symptoms have dramatically improved and the window for potential “rebound effect” from racemic epinephrine has passed with no further stridor.
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Nussbaumer-Ochsner, Yvonne, and Konrad E. Bloch. Sleep at high altitude and during space travel. Edited by Sudhansu Chokroverty, Luigi Ferini-Strambi, and Christopher Kennard. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199682003.003.0054.
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This chapter summarizes data on sleep–wake disturbances in humans at high altitude and in space. High altitude exposure is associated with periodic breathing and a trend toward reduced slow-wave sleep and sleep efficiency in healthy individuals. Some subjects are affected by altitude-related illness (eg, acute and chronic mountain sickness, high-altitude cerebral and pulmonary edema). Several drugs are available to prevent and treat these conditions. Data about the effects of microgravity on sleep are limited and do not allow the drawing of firm conclusions. Microgravity and physical and psychological factors are responsible for sleep–wake disturbances during space travel. Space missions are associated with sleep restriction and disruption and circadian rhythm disturbances encouraging use of sleep medication. An unexplained and unexpected finding is the improvement in upper airway obstructive breathing events and snoring during space flight.
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Karon, Barry L., and Naveen L. Pereira. Heart Failure and Cardiomyopathies. Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780199755691.003.0046.
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Heart failure is a clinical syndrome characterized by the inability of the heart to maintain adequate cardiac output to meet the metabolic demands of the body while still maintaining normal or near-normal ventricular filling pressures. Heart failure may be present at rest, but often it is present only during exertion as a result of the dynamic nature of cardiac demands. For correct treatment of heart failure, the mechanism, underlying cause, and any reversible precipitating factors must be identified. Typical manifestations of heart failure are dyspnea and fatigue that limit activity tolerance and fluid retention leading to pulmonary or peripheral edema. The most recent proposed categorization divided the cardiomyopathies into primary and secondary cardiomyopathies, and the primary disorders are further subdivided as genetic, acquired, or mixed. Although this proposal takes into account our progressive understanding of this heterogeneous group of disorders, the previous phenotypic classification of dilated, hypertrophic, and restrictive diseases still provides utility in day-to-day understanding and management of these disorders.
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Albright, Robert C. Acid-Base and Electrolyte Disorders. Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780199755691.003.0474.
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The most important principle in understanding disorders of water balance is that sodium balance is determined by the adequacy of the effective circulating volume, while water balance is determined by osmoregulation and the interplay between vasopressin activity, renal concentrating and diluting ability, and thirst. Disorders of sodium balance can be determined only by clinical examination. Orthostatic hypotension implies volume depletion and sodium deficiency. Edema implies volume excess and sodium excess. Potassium is predominantly an intracellular cation. The intracellular balance of potassium is regulated by endogenous factors such as acidemia, sodium, adenosine triphosphatase, insulin, catecholamines, and aldosterone. Clinically, it is absolutely critical to follow a stepwise approach to acid-base disorders. Metabolic acidosis is defined as a primary disturbance in which the retention of acid consumes endogenous alkali stores. This is reflected by a decrease in bicarbonate. Metabolic alkalosis is defined as a primary disturbance in which plasma bicarbonate is increased. The signs and symptoms of metabolic alkalosis include weakness, muscle cramps, hyperreflexia, alveolar hypoventilation, and arrhythmias.
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Vásquez Bajaña, Viviana Beatriz, Madeleine Juliana Sarmiento Cabrera, Génesis Carolina Romoleroux Uquillas, Maite Guisella Santillan Arias, Pamela Elena Salas Espín, Yosselin Yolanda Gualancañay Zurita, Cirlei Elizabeth Pita Aveiga, et al. Introducción a la Medicina Interna: Conceptos fundamentales. Mawil Publicaciones de Ecuador, 2022, 2022. http://dx.doi.org/10.26820/978-9942-602-44-2.
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En este libro «Introducción a la medicina interna» se ofrece al lector información actualizada sobre diversos temas referentes a patologías que cursan como causa principal de alta morbimortalidad en el mundo contemporáneo. Todos de gran interés y vital importancia para la preservación de la salud. En el capítulo I, se enfoca en la discusión de los «conceptos elementales» relacionados con la medicina interna, las competencias profesionales del médico internista y la bioética en la práctica médica. En el capítulo II, se aborda el tema de las «enfermedades del sistema cardiovascular». Entre estas: La epidemiología de la enfermedad cardiovascular, los factores de riesgo de las enfermedades cardiovasculares, la hipertensión arterial, el edema agudo del pulmón, el paro cardiaco y la reanimación. En el capítulo III, se exponen algunas de las principales «enfermedades del sistema respiratorio». En primer lugar, se describe el aparato respiratorio humano, para seguidamente hacer referencia a la historia clínica en las patologías respiratorias y exponer con detalle la enfermedad pulmonar obstructiva crónica, el derrame plural y la disnea.
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Eimanis, Mārcis. Usage of Double-Helical Propulsion Principle in Underwater Vehicles. RTU Press, 2022. http://dx.doi.org/10.7250/9789934227370.
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The Thesis describes a new underwater vehicle propulsion type developed by the author. Flow and vehicle interaction dynamics are studied, and factors impacting the flow, control methods and the ability to move in other media (in addition to fluid) are reviewed. A geometry of the propulsion system was created by studying its hydrodynamic properties using special CFD software. A mathematical model for the control system was created. The dynamics of the underwater vehicle were modelled with the multibody dynamics modelling software MSC Adams, using the developed control system and the water resistance model developed with CFD software. Flow dynamics were combined with multibody mechanism dynamics using the metamodeling and numerical experiment approach. Numerical experiments in bulk or granular media were performed using the discrete element method, simulating the vehicle movement using the EDEM software. Within the framework of the Thesis, a prototype of the model was also created for observing the model behaviour in real-life conditions. High-quality and good fit results were obtained from the mathematical model and the physical prototype dynamics, proving the performance of both the new propulsion principle and the control system.
Book chapters on the topic "Edema factor"
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Takeuchi, Satoru, Kimihiro Nagatani, Kojiro Wada, Hiroshi Nawashiro, Naoki Otani, Hideo Osada, Hiroaki Kobayashi, Takamoto Suzuki, and Katsuji Shima. "Is Decompressive Craniectomy a Risk Factor for Ventriculomegaly?" In Brain Edema XV, 281–83. Vienna: Springer Vienna, 2013. http://dx.doi.org/10.1007/978-3-7091-1434-6_54.
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Fukui, S., Hiroshi Nawashiro, N. Otani, H. Ooigawa, A. Yano, N. Nomura, A. M. Tokumaru, et al. "Vascular endothelial growth factor expression in pituitary adenomas." In Brain Edema XII, 519–21. Vienna: Springer Vienna, 2003. http://dx.doi.org/10.1007/978-3-7091-0651-8_106.
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Davidson, Max, and Aman Chandra. "Anti-Vascular Endothelial Growth Factor Agents for Diabetic Macular Edema." In Diabetic Macular Edema, 55–61. Singapore: Springer Nature Singapore, 2022. http://dx.doi.org/10.1007/978-981-19-7307-9_6.
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Tokutomi, Takashi, M. Sigemori, T. Kikuchi, and M. Hirohata. "Effect of Platelet-Activating Factor Antagonist on Brain Injury in Rats." In Brain Edema IX, 508–10. Vienna: Springer Vienna, 1994. http://dx.doi.org/10.1007/978-3-7091-9334-1_139.
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Yin, L., H. Ohtaki, T. Nakamachi, K. Dohi, Y. Iwai, H. Funahashi, R. Makino, and Seiji Shioda. "Expression of tumor necrosis factor α (TNFα) following transient cerebral ischemia." In Brain Edema XII, 93–96. Vienna: Springer Vienna, 2003. http://dx.doi.org/10.1007/978-3-7091-0651-8_21.
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Tsuzuki, N., T. Miyazawa, K. Matsumoto, T. Nakamura, K. Shima, and H. Chigasaki. "Hepatocyte Growth Factor Reduces Infarct Volume After Transient Focal Cerebral Ischemia in Rats." In Brain Edema XI, 311–16. Vienna: Springer Vienna, 2000. http://dx.doi.org/10.1007/978-3-7091-6346-7_64.
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Verma, Aditya, Yamini Attiku, and Srinivas R. Sadda. "Endpoints of Anti-Vascular Endothelial Growth Factor Clinical Trials for Diabetic Macular Edema." In Diabetic Macular Edema, 185–98. Singapore: Springer Nature Singapore, 2022. http://dx.doi.org/10.1007/978-981-19-7307-9_16.
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Ohnishi, T., T. Hayakawa, and W. R. Shapiro. "Human Malignant Gliomas Secrete a Factor that Increases Brain Capillary Permeability: Role in Peritumoural Brain Oedema." In Brain Edema VIII, 137–39. Vienna: Springer Vienna, 1990. http://dx.doi.org/10.1007/978-3-7091-9115-6_46.
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Suzuki, Ryuta, N. Fukai, G. Nagashijma, J. I. Asai, H. Itokawa, M. Nagai, T. Suzuki, and T. Fujimoto. "Very early expression of vascular endothelial growth factor in brain oedema tissue associated with brain contusion." In Brain Edema XII, 277–79. Vienna: Springer Vienna, 2003. http://dx.doi.org/10.1007/978-3-7091-0651-8_60.
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Taylor, Aubrey E., James C. Parker, and Bengt Rippe. "Edema and the Tissue Resistance Safety Factor." In Tissue Nutrition and Viability, 185–95. New York, NY: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4684-0629-0_9.
Full textConference papers on the topic "Edema factor"
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Donaldson, V. H., and M. D. B. H. Mitchell. "INTERACTIONS OF DYSFUNCTIONAL Cl-INHIBITORS FROM PATIENTS WITH TYPE II HEREDITARY ANGIONEUROTIC EDEMA (HANE) WITH ACTIVATED HAGEMAN FACTOR (FACTOR XIIa)." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643302.
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Type II HANE is characterized by a deficiency of Cl-inhibitor (Cl-INH) activity in serum which is associated with a dysfunctional inhibitor protein having a normal or increased quantity o|_the antigenic properties of normal serum Cl-inhibitor. Dysfunctional Cl-INH proteins were purified from members_of eight different kindred with Type II HANE and compared to normal Cl-inhibitor with respect to their inhibitory activity directed against the amidolytic and clot-promoting properties of purified activated Hageman factor. All but one dysfunctional Cl-inhibitor blocked the amidolytic activity of ellagic acid-activated Hageman factor; all eight blocked the clot-promoting activity of Hageman factor activated in solutions of sulfatides and BSA. The inhibition _of amidolytic activity was equal to or greater than that of normal Cl-INH (Donaldson, et al., 3. Clin. Invest. 75:124,1985). The impairment of the specific Hageman factor coagulant activity of activated Hageman factor by six^f the eight dysfunctional inhibitors was less than that of the normal Cl-inhibitor, although readily measured. Dysfunctional Cl-inhibitor proteins were also heterogeneous with respect to their formation of stable complexes and their susceptibility to cleavage by Hageman factor activated with BSA-sulfatides when analyzed in SDS-gel electrophoresis. Although these observatons cannot be directly applied to in vivo pathophysiologic changes in plasma, dysfunctional Cl-inhibitors do have the potential of regulating activated Hageman factor.
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Bai, Chunxue, Jun She, Yuanlin Song, Lin Tong, and Jing Bi. "Prophylactic Use Of Keratinocyte Growth Factor-2 Distinctly Prevents High Altitude Pulmonary Edema In Rats." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a3775.
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She, Jun, Yuanlin Song, and Chunxue Bai. "Keratinocyte Growth Factor-2 Targets Alveolar Epithelial And Capillary Endothelial To Reduce High Altitude Pulmonary Edema." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a6379.
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Semenov, Sergey, Alexandr Bozhchenko, and Pavel Tolkach. "Iatrogenic death of a patient as a result of local anesthesia with the use of the drug “Naropin”." In Issues of determining the severity of harm caused to human health as a result of the impact of a biological factor. ru: Publishing Center RIOR, 2020. http://dx.doi.org/10.29039/conferencearticle_5fdcb03ab42468.53224529.
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The article considers the clinical and forensic aspects of the possibility of establishing a causal relationship between the use of the drug “Naropin” and the death of a patient during local anesthesia. In this case, the patient sought outpatient medical care for paraproctitis. The decision made by the doctor the decision for local anesthesia is the use of the drug “Naropin”. At 20 minutes of administration of the drug in the required dosage, the patient suddenly developed convulsions and clinical death occurred, and later the patient died. When conducting a forensic examination of the corpse, the most significant was the following: a small pinpoint wound in the upper quadrant of the right buttock, pulmonary edema, liquid blood and small loose blood clots in the heart cavities, brain edema. During a post-mortem Toxicological examination of the blood, the presence of ropivacaine (a component of naropine) was found to exceed the threshold toxic concentration. Repeated expert research has found that led to the onset of death-the erroneous introduction of the anesthetic “Naropin” directly into the blood vessel, which is prohibited by the instructions for its use due to a very narrow zone of toxic action.
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Suzuki, R., and Y. Takamura. "COAGULATION FINDINGS IN ULCERATIVE COLITIS AND THE BENEFICIAL EFFECT OF FACTOR XIII CONCENTRATE SUBSTITUTION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643308.
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Reports suggest that there is a tendency towards hypercoagulability in ulcerative colitis (UC). However, few reports deal with factor XIII which plays an important role in the wound healing process.In the present study, 8 coagulation parameters including factor XIII activity were determined in 5 patients with UC at the active stage and in 15 patients at remission. A comparison of the two groups shows that, in the active-stage patients, the levels of factor XIII activity were significantly lower, platelets and fibrinogen higher, and the PT prolonged.Furthermore, Factor XIII concentrate (Fibrogammin P ) was administered to 4 patients with active-stage UC and abdominal symptoms. Here, the symptoms (i.e. abdominal pain, melaena, diarrhea, etc.) disappeared in accordance with the increase in factor XIII activity. Endoscopyprevealed that treatment with factor XIII concentrate (Fibrogammin P ) had a beneficial effect on mucosal edema, redness and hemorrhage as well as on healing of erosions and ulcars.The results suggest that the level of factor XIII activity is a remarkably good measure of the severity of UC and that administration of factor XIII concentrate may be useful for treatment.
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Ley, Obdulia, and Yildiz Bayazitoglu. "Effect of Physiological Parameters on the Temperature Distribution of a Layered Head Model." In ASME 2002 International Mechanical Engineering Congress and Exposition. ASMEDC, 2002. http://dx.doi.org/10.1115/imece2002-32044.
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Brain temperature control is important in clinical therapy, because moderate temperature reduction of brain temperature increases the survival rate after head trauma. A factor that affects the brain temperature distribution is the cerebral blood flow, which is controlled by autoregulatory mechanisms. To improve the existing thermal models of brain, we incorporate the effect of the temperature over the metabolic heat generation, and the regulatory processes that control the cerebral blood perfusion and depend on physiological parameters like, the mean arterial blood pressure, the partial pressure of oxygen, the partial pressure of carbon dioxide, and the cerebral metabolic rate of oxygen consumption. The introduction of these parameters in a thermal model gives information about how specific conditions, such as brain edema, hypoxia, hypercapnia, or hypotension, affect the temperature distribution within the brain. Existing biological thermal models of the human brain, assume constant blood perfusion, and neglect metabolic heat generation or consider it constant, which is a valid assumption for healthy tissue. But during sickness, trauma or under the effect of drugs like anesthetics, the metabolic activity and organ blood flow vary considerably, and such variations must be accounted for in order to achieve accurate thermal modeling. Our work, on a layered head model, shows that variations of the physiological parameters have profound effect on the temperature gradients within the head.
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Kim, Jin Hee (Heather), Joan Stilling, Michael O'Dell, and Cindy Hsin-Liu Kao. "KnitDema: Robotic Textile as Personalized Edema Mobilization Device." In CHI '23: CHI Conference on Human Factors in Computing Systems. New York, NY, USA: ACM, 2023. http://dx.doi.org/10.1145/3544548.3581343.
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Leite, Izabel Feitosa da Mata, Adelina Mouta Moreira Neto, Guilherme de Aguiar Moraes, Lucas Cardoso Siqueira Albernaz, and Matheus de Campos Medeiros. "Neuro-Behçet’s Syndrome: case report." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.209.
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Context: Behçet’s Disease (BD) is a multisystem chronic disorder characterized by perivasculitis within several tissues, including the Central Nervous System – Neuro-Behçet’s Disease, which accounts for 3 – 9 % of the BD patients. Neuro- Behçet’s Syndrome may present as brainstem or pyramidal syndromes, myelopathies, meningoencephalitis, intracranial hypertension and movement or psychiatric disorders. The objective of the present work is to report a case of Neuro-Behçet’s Disease, a rare and disabling disorder. Case report: 24-year-old male presenting focal neurological deficits – hemiparesis on the right side and motor aphasia, associated with unstoppable hiccups and visual blurring. His previous pathological history featured several self-limiting episodes of the same neurological presentation, as well as acute exacerbations of oral and genital ulcers. Erythema Nodosum and Folliculitis were his main skin lesions. The ophthalmological evaluation showed bilateral cicatricial chorioretinitis. Laboratorial diagnostic procedures revealed left shift leukocytosis, high ESR, high protein level in the CSF and negative serology for B and C hepatitis, HTLV, HIV and toxoplasmosis. P-ANCA, C-ANCA, ANA and Rheumatoid factor were all found negative. Magnetic Resonance Imaging of the brain showed multiple oval- shaped T2- hyperintensity foci, with adjacent vasogenic edema, in the brainstem and basal ganglia areas – suggesting vasculitis. Treatment involved pulse therapy with Methylprednisolone, followed by Azathioprine and Prednisone. The patient has had full recovery and no other relapses. Conclusions: This case illustrates the importance of investigating Neuro-Behçet’s Disease in patients with neurological symptoms and oral/genital ulcers. The goal is to establish adequate and early treatment to improve the quality of life.
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Mota, Geovana Souza, Julia Cortapassi Amaral Vilela, and Amandra Gabriele Coelho Rodrigues Melo. "Aneurysm in the vein of galenus in a newborn: case report." In XIV Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2023. http://dx.doi.org/10.5327/1516-3180.141s1.678.
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Case presentation: M.L.S, 17-year-old, G1P0A0, 35 weeks, referred to the pediatric neurosurgery service for prenatal evaluation and postpartum surgical planning because the fetus has ventricular asymmetry on initial ultrasound examination. Previously the mother had no morphological ultrasound and no proper prenatal care, she was referred to the neurosurgery service but did not attend the appointment, which made it difficult to transfer to an appropriate hospital. After the initial examination, she underwent magnetic resonance imaging, a fetal morphology study and transcranial Doppler ultrasound that showed the presence of a bulky expandable mass compatible with a galenary vein aneurysm. The patient presented pulmonary hypertension that made surgical intervention impossible and died on the 12th day of life due to refractory heart failure. Case discussion: Galen’s vein has a great importance because it drains the central portion of the brain. Prenatal developmental aneurysmal malformation of the gallenary vein begins in the first trimester of gestation, with variable severity and clinical manifestations that can manifest intrauterine with signs of heart failure, hydrocephalus or oligohydramnios. The patient evolved with significant respiratory distress and acute pulmonary edema abs the severity of the condition made it impossible to perform the surgery. Vein of Galen aneurysm constitutes less than 1% of the cases of congenital vascular malformation, its early diagnosis is of great importance, especially since the condition has a high lethality rate. The recognition of this condition based on ultrasound in the prenatal period is a fundamental factor for the diagnosis of the aneurysm and its subsequent referral to a reference center. In this way it is possible to define the best treatment model. Conclusion: It is assumed that if it were diagnosed and referred properly during the intrauterine period, it would be possible to evolve successfully and diminish or nullify the pathophysiological consequences of the newborn aneurysm of Galen’s vein.
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Chopra, Aman, Ashray Dimri, and Tribikram Pradhan. "Prediction of factors affecting amlodipine induced pedal edema and its classification." In 2017 International Conference on Advances in Computing, Communications and Informatics (ICACCI). IEEE, 2017. http://dx.doi.org/10.1109/icacci.2017.8126085.
Full textReports on the topic "Edema factor"
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Motin, V., E. Garcia, D. Barsky, and A. Zemla. Novel Yersinia Pestis Toxin that Resembles Bacillus Anthracis Edema Factor: Study of Activity and Structural Modeling. Office of Scientific and Technical Information (OSTI), February 2003. http://dx.doi.org/10.2172/15003020.
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Liu, Kun, Jing Wu, Xiaoning He, Jia Liu, and Fang Qi. Anti-Vascular Endothelial Growth Factor (anti-VEGF) for Diabetic Macular Edema (DME): A Systematic Review and Network Meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, June 2021. http://dx.doi.org/10.37766/inplasy2021.6.0009.
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Arévalo-Sáenz, Alejandra, Borja Ferrández Pujante, and Fernando J. Rascón-Ramírez. Peritumoral Edema in Resected Meningiomas: Study of Factors Associated with the Variability of Postoperative Duration. Science Repository, March 2024. http://dx.doi.org/10.31487/j.scr.2024.01.05.
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Background: It is well known that edema can persist after meningioma resection, and sometimes it is not resolved after this time. This study aimed to establish the relationship between a series of variables associated with meningioma or surgery, and the duration of postoperative edema. Methods: We conducted a retrospective study of 77 meningiomas resected at our institution between January 2016 and January 2018 with a maximum follow-up period of up to three years. The independent variables collected were demographics, tumor location, relationship with the sinuses (invasion/contact), relationship with arterial structures, deviation from the midline, volume (cm3), degree of initial edema, WHO histological classification, degree of atypia, degree of resection, previous embolization, and development of complications. The edema levels were classified according to the classification described by Ide et al. (1995): GR0, GR1, and GR2. Measurements were performed using FLAIR magnetic resonance sequences. Statistical analyses were performed using the SPSS 21. Results: Age (p=0.003), deviation from the midline (p=0.001), and tumor volume (p<0.001) were correlated with outcome using Spearman's test. Univariate analysis revealed that the localization (p=0.016), initial edema (p<0.001), degree of atypia (p=0.019), and presence of previous embolization (p=0.037) were statistically significant. In multivariate analysis, only age, initial edema, and embolization were significant independent predictors. Conclusion: These results suggest that the degree of initial edema, midline deviation, tumor volume, tumor location, degree of atypia, and previous embolization may be important predictors of postoperative edema duration.