Literatura académica sobre el tema "Edema factor"
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Artículos de revistas sobre el tema "Edema factor"
Hirashima, Yutaka, Nakamasa Hayashi, Osamu Fukuda, Hideki Ito, Shunro Endo y Akira Takaku. "Platelet-activating factor and edema surrounding meningiomas". Journal of Neurosurgery 88, n.º 2 (febrero de 1998): 304–7. http://dx.doi.org/10.3171/jns.1998.88.2.0304.
Texto completoSeifert, Roland y Stefan Dove. "Inhibitors of Bacillus anthracis edema factor". Pharmacology & Therapeutics 140, n.º 2 (noviembre de 2013): 200–212. http://dx.doi.org/10.1016/j.pharmthera.2013.07.002.
Texto completoChen, Deliang, Milind Misra, Laurie Sower, Johnny W. Peterson, Glen E. Kellogg y Catherine H. Schein. "Novel inhibitors of anthrax edema factor". Bioorganic & Medicinal Chemistry 16, n.º 15 (agosto de 2008): 7225–33. http://dx.doi.org/10.1016/j.bmc.2008.06.036.
Texto completoVilleco, June P. "Edema: A Silent but Important Factor". Journal of Hand Therapy 25, n.º 2 (abril de 2012): 153–62. http://dx.doi.org/10.1016/j.jht.2011.09.008.
Texto completoPost, Michał, Dorota Polakowska, Dominika Wróbel-Dudzińska y Jacek P. Szaflik. "Therapeutic Approaches for Treatment of Diabetic Macular Edema". Ophthalmology, n.º 3 (30 de diciembre de 2023): 26–31. http://dx.doi.org/10.5114/oku/178041.
Texto completoFirstova, V. V., I. G. Shemyakin y 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, n.º 5-6 (1 de febrero de 2020): 639–47. http://dx.doi.org/10.15789/2220-7619-2019-5-6-639-647.
Texto completoBrunelle, Cheryl L., Meyha N. Swaroop, Melissa N. Skolny, Maria S. Asdourian, Hoda E. Sayegh y Alphonse G. Taghian. "Hand Edema in Patients at Risk of Breast Cancer–Related Lymphedema: Health Professionals Should Take Notice". Physical Therapy 98, n.º 6 (18 de enero de 2018): 510–17. http://dx.doi.org/10.1093/ptj/pzy007.
Texto completoBerthiaume, Yves. "Tumor Necrosis Factor and Lung Edema Clearance". American Journal of Respiratory and Critical Care Medicine 168, n.º 9 (noviembre de 2003): 1022–23. http://dx.doi.org/10.1164/rccm.2308003.
Texto completoJiao, Guan-Sheng, Seongjin Kim, Mahtab Moayeri, April Thai, Lynne Cregar-Hernandez, Linda McKasson, Sean O'Malley, Stephen H. Leppla y Alan T. Johnson. "Small molecule inhibitors of anthrax edema factor". Bioorganic & Medicinal Chemistry Letters 28, n.º 2 (enero de 2018): 134–39. http://dx.doi.org/10.1016/j.bmcl.2017.11.040.
Texto completoLeysath, Clinton E., Kuang-Hua Chen, Mahtab Moayeri, Devorah Crown, Rasem Fattah, Zhaochun Chen, Suman R. Das, Robert H. Purcell y Stephen H. Leppla. "Mouse Monoclonal Antibodies to Anthrax Edema Factor Protect against Infection". Infection and Immunity 79, n.º 11 (12 de septiembre de 2011): 4609–16. http://dx.doi.org/10.1128/iai.05314-11.
Texto completoTesis sobre el tema "Edema factor"
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/.
Texto completoBhandari, Sanjeeb. "Real-world Treatment Outcomes for Diabetic Macular Edema". Thesis, University of Sydney, 2020. https://hdl.handle.net/2123/24071.
Texto completoGómez, 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.
Texto completoRATIONALE: 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.
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.
Texto completoIntroduction: 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
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.
Texto completoThe 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.
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.
Texto completoEdema 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
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.
Texto completoDiabetic 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.
McCafferty, Sean, April Harris, Corin Kew, Tala Kassm, Lisa Lane, Jason Levine y 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.
Texto completoRud, 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.
Texto completoFigueras, 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.
Texto completoINTRODUCTION: 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.
Libros sobre el tema "Edema factor"
Davison, Earl. Macular Edema: Risk Factors, Treatment Options and Long-Term Outcomes. Nova Science Publishers, Incorporated, 2014.
Buscar texto completoLoochtan, Aaron I., Jodi Dodds y Cheryl D. Bushnell. Hemorrhagic Stroke Management in Pregnancy. Editado por Emma Ciafaloni, Cheryl Bushnell y Loralei L. Thornburg. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190667351.003.0015.
Texto completoBaijal, Rahul y Carlos J. Campos. Diabetic Ketoacidosis in a Child with Acute Surgical Abdomen. Editado por Erin S. Williams, Olutoyin A. Olutoye, Catherine P. Seipel y Titilopemi A. O. Aina. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190678333.003.0040.
Texto completoGore, Cheryl, Junzheng Wu y C. Dean Kurth. Stridor after Extubation. Editado por Erin S. Williams, Olutoyin A. Olutoye, Catherine P. Seipel y Titilopemi A. O. Aina. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190678333.003.0066.
Texto completoNussbaumer-Ochsner, Yvonne y Konrad E. Bloch. Sleep at high altitude and during space travel. Editado por Sudhansu Chokroverty, Luigi Ferini-Strambi y Christopher Kennard. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199682003.003.0054.
Texto completoKaron, Barry L. y Naveen L. Pereira. Heart Failure and Cardiomyopathies. Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780199755691.003.0046.
Texto completoAlbright, Robert C. Acid-Base and Electrolyte Disorders. Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780199755691.003.0474.
Texto completoVásquez 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.
Texto completoEimanis, Mārcis. Usage of Double-Helical Propulsion Principle in Underwater Vehicles. RTU Press, 2022. http://dx.doi.org/10.7250/9789934227370.
Texto completoCapítulos de libros sobre el tema "Edema factor"
Takeuchi, Satoru, Kimihiro Nagatani, Kojiro Wada, Hiroshi Nawashiro, Naoki Otani, Hideo Osada, Hiroaki Kobayashi, Takamoto Suzuki y Katsuji Shima. "Is Decompressive Craniectomy a Risk Factor for Ventriculomegaly?" En Brain Edema XV, 281–83. Vienna: Springer Vienna, 2013. http://dx.doi.org/10.1007/978-3-7091-1434-6_54.
Texto completoFukui, S., Hiroshi Nawashiro, N. Otani, H. Ooigawa, A. Yano, N. Nomura, A. M. Tokumaru et al. "Vascular endothelial growth factor expression in pituitary adenomas". En Brain Edema XII, 519–21. Vienna: Springer Vienna, 2003. http://dx.doi.org/10.1007/978-3-7091-0651-8_106.
Texto completoDavidson, Max y Aman Chandra. "Anti-Vascular Endothelial Growth Factor Agents for Diabetic Macular Edema". En Diabetic Macular Edema, 55–61. Singapore: Springer Nature Singapore, 2022. http://dx.doi.org/10.1007/978-981-19-7307-9_6.
Texto completoTokutomi, Takashi, M. Sigemori, T. Kikuchi y M. Hirohata. "Effect of Platelet-Activating Factor Antagonist on Brain Injury in Rats". En Brain Edema IX, 508–10. Vienna: Springer Vienna, 1994. http://dx.doi.org/10.1007/978-3-7091-9334-1_139.
Texto completoYin, L., H. Ohtaki, T. Nakamachi, K. Dohi, Y. Iwai, H. Funahashi, R. Makino y Seiji Shioda. "Expression of tumor necrosis factor α (TNFα) following transient cerebral ischemia". En Brain Edema XII, 93–96. Vienna: Springer Vienna, 2003. http://dx.doi.org/10.1007/978-3-7091-0651-8_21.
Texto completoTsuzuki, N., T. Miyazawa, K. Matsumoto, T. Nakamura, K. Shima y H. Chigasaki. "Hepatocyte Growth Factor Reduces Infarct Volume After Transient Focal Cerebral Ischemia in Rats". En Brain Edema XI, 311–16. Vienna: Springer Vienna, 2000. http://dx.doi.org/10.1007/978-3-7091-6346-7_64.
Texto completoVerma, Aditya, Yamini Attiku y Srinivas R. Sadda. "Endpoints of Anti-Vascular Endothelial Growth Factor Clinical Trials for Diabetic Macular Edema". En Diabetic Macular Edema, 185–98. Singapore: Springer Nature Singapore, 2022. http://dx.doi.org/10.1007/978-981-19-7307-9_16.
Texto completoOhnishi, T., T. Hayakawa y W. R. Shapiro. "Human Malignant Gliomas Secrete a Factor that Increases Brain Capillary Permeability: Role in Peritumoural Brain Oedema". En Brain Edema VIII, 137–39. Vienna: Springer Vienna, 1990. http://dx.doi.org/10.1007/978-3-7091-9115-6_46.
Texto completoSuzuki, Ryuta, N. Fukai, G. Nagashijma, J. I. Asai, H. Itokawa, M. Nagai, T. Suzuki y T. Fujimoto. "Very early expression of vascular endothelial growth factor in brain oedema tissue associated with brain contusion". En Brain Edema XII, 277–79. Vienna: Springer Vienna, 2003. http://dx.doi.org/10.1007/978-3-7091-0651-8_60.
Texto completoTaylor, Aubrey E., James C. Parker y Bengt Rippe. "Edema and the Tissue Resistance Safety Factor". En Tissue Nutrition and Viability, 185–95. New York, NY: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4684-0629-0_9.
Texto completoActas de conferencias sobre el tema "Edema factor"
Donaldson, V. H. y 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)." En XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643302.
Texto completoBai, Chunxue, Jun She, Yuanlin Song, Lin Tong y Jing Bi. "Prophylactic Use Of Keratinocyte Growth Factor-2 Distinctly Prevents High Altitude Pulmonary Edema In Rats". En 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.
Texto completoShe, Jun, Yuanlin Song y Chunxue Bai. "Keratinocyte Growth Factor-2 Targets Alveolar Epithelial And Capillary Endothelial To Reduce High Altitude Pulmonary Edema". En 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.
Texto completoSemenov, Sergey, Alexandr Bozhchenko y Pavel Tolkach. "Iatrogenic death of a patient as a result of local anesthesia with the use of the drug “Naropin”". En 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.
Texto completoSuzuki, R. y Y. Takamura. "COAGULATION FINDINGS IN ULCERATIVE COLITIS AND THE BENEFICIAL EFFECT OF FACTOR XIII CONCENTRATE SUBSTITUTION." En XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643308.
Texto completoLey, Obdulia y Yildiz Bayazitoglu. "Effect of Physiological Parameters on the Temperature Distribution of a Layered Head Model". En ASME 2002 International Mechanical Engineering Congress and Exposition. ASMEDC, 2002. http://dx.doi.org/10.1115/imece2002-32044.
Texto completoKim, Jin Hee (Heather), Joan Stilling, Michael O'Dell y Cindy Hsin-Liu Kao. "KnitDema: Robotic Textile as Personalized Edema Mobilization Device". En CHI '23: CHI Conference on Human Factors in Computing Systems. New York, NY, USA: ACM, 2023. http://dx.doi.org/10.1145/3544548.3581343.
Texto completoLeite, Izabel Feitosa da Mata, Adelina Mouta Moreira Neto, Guilherme de Aguiar Moraes, Lucas Cardoso Siqueira Albernaz y Matheus de Campos Medeiros. "Neuro-Behçet’s Syndrome: case report". En XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.209.
Texto completoMota, Geovana Souza, Julia Cortapassi Amaral Vilela y Amandra Gabriele Coelho Rodrigues Melo. "Aneurysm in the vein of galenus in a newborn: case report". En XIV Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2023. http://dx.doi.org/10.5327/1516-3180.141s1.678.
Texto completoChopra, Aman, Ashray Dimri y Tribikram Pradhan. "Prediction of factors affecting amlodipine induced pedal edema and its classification". En 2017 International Conference on Advances in Computing, Communications and Informatics (ICACCI). IEEE, 2017. http://dx.doi.org/10.1109/icacci.2017.8126085.
Texto completoInformes sobre el tema "Edema factor"
Motin, V., E. Garcia, D. Barsky y 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), febrero de 2003. http://dx.doi.org/10.2172/15003020.
Texto completoLiu, Kun, Jing Wu, Xiaoning He, Jia Liu y 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, junio de 2021. http://dx.doi.org/10.37766/inplasy2021.6.0009.
Texto completoArévalo-Sáenz, Alejandra, Borja Ferrández Pujante y Fernando J. Rascón-Ramírez. Peritumoral Edema in Resected Meningiomas: Study of Factors Associated with the Variability of Postoperative Duration. Science Repository, marzo de 2024. http://dx.doi.org/10.31487/j.scr.2024.01.05.
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