Journal articles: '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.

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Fujii, Yu, Toshihiro Ogiwara, Masahiro Agata, Yoshiki Hanaoka, and Tetsuyoshi Horiuchi. "STMO-01 Cerebral edema and perioperative epilepsy due to placement of BCNU wafer for malignant glioma." Neuro-Oncology Advances 2, Supplement_3 (November 1, 2020): ii9. http://dx.doi.org/10.1093/noajnl/vdaa143.039.

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Abstract Introduction: Cerebral edema is the most frequent adverse event of BCNU wafer, which is used as local chemotherapy of malignant glioma. However, predictive factor of this event is unknown. Moreover, there is no consensus about cerebral edema and perioperative seizure, which is often observed in glioma. Here, we report risk factor of cerebral edema with BCNU placement and relationship with perioperative seizure in malignant glioma cases. Material and Method: Thirty-one case of adult malignant glioma who underwent BCNU placement in our institute between March 2013 to March 2019 were investigated. The patients were dichotomized to two groups; patient with postoperative transient cerebral edema (CE+ group) and patient without postoperative transient cerebral edema (CE- group). Result: Postoperative cerebral edema associated with placement of BCNU was observed in 9 out of 31 patients (29%). Tumor malignancy was significant parameter for postoperative cerebral edema (p=0.003). Other factors such as, age, gender, laterality, tumor location, primary or recurrent, number of BCNU wafers, duration of recurrence were not significant for postoperative cerebral edema. Seizure was seen in 14 patients (45%), and cerebral edema was not significant parameter for seizure. Tumor malignancy was significant parameters for postoperative cerebral edema. Tumor malignancy was significant parameters for seizure (p=0.0004). Although postoperative seizure was observed in 4 patients (44%) with CE+ group, neither maximum volume (mean 61.1 ml) nor change ratio (mean 354%) of FLAIR-high-intensity region were not related with postoperative seizure. Conclusions: Tumor malignancy was important factor for patients who underwent placement of BCNU wafer with postoperative cerebral edema and seizure. On the other hand, there were no relationship between postoperative cerebral edema and perioperative seizure in patients treated with BCNU wafer.

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Kalkanis, Steven N., Rona S. Carroll, Jianping Zhang, Amir A. Zamani, and Peter McL Black. "Correlation of vascular endothelial growth factor messenger RNA expression with peritumoral vasogenic cerebral edema in meningiomas." Journal of Neurosurgery 85, no. 6 (December 1996): 1095–101. http://dx.doi.org/10.3171/jns.1996.85.6.1095.

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✓ Intracranial meningiomas are often complicated by peritumoral vasogenic cerebral edema, which appears to result from increased microvascular permeability and extravasation of proteinaceous and plasma fluid into the adjacent peritumoral space. The source of such edema has long been mysterious. The contents of this paper support the concept that vascular endothelial growth factor (VEGF) production plays a significant role in edema formation. Vascular endothelial growth factor messenger RNA expression has been found in a wide range of intracranial neoplasms, including malignant gliomas, metastatic melanomas, meningiomas, and other benign tumors. Several studies have confirmed the importance of VEGF in tumorigenesis, neovascularization, and edema production. This study tests the hypothesis that the presence of peritumoral edema in meningiomas is positively correlated with increased expression of VEGF mRNA. To investigate this hypothesis, 31 meningioma specimens were subjected to Northern blot analysis, hybridization with a complementary DNA VEGF probe, and laser densitometry to determine the relative levels of VEGF mRNA expression. Magnetic resonance imaging was then used in a double-blind fashion to correlate the neuropathological tissue samples with the presence of preoperative peritumoral edema. Of 31 patients studied, 14 exhibited no edema and 17 exhibited some level of peritumoral fluid accumulation. There was a marked increase in VEGF expression in patients with edema (p = 0.0004, Wilcoxon-Mann-Whitney rank-sum test). Meningiomas with peritumoral edema exhibited 3.4 times the level of VEGF mRNA as those without edema. These data demonstrate a strong link between VEGF mRNA expression and peritumoral edema and indicate that VEGF expression is an important factor in the etiology of edema around meningiomas.

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Carroll, Robert M., Yinxi Yu, and Brian L. VanderBeek. "Predictive factors for patients receiving intravitreal anti-vascular endothelial growth factor for the treatment of diabetic macular edema." European Journal of Ophthalmology 30, no. 1 (February 14, 2019): 72–80. http://dx.doi.org/10.1177/1120672119827856.

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Purpose: To determine whether anemia and other demographic or laboratory “risk factors” impact anti-vascular endothelial growth factor treatment in diabetic macular edema patients. Methods: This is a retrospective, time-varying cohort study using a medical claims database to identify new diabetic macular edema patients who had received at least one intravitreal injection of anti-vascular endothelial growth factor. Exclusion occurred for having <2 years in the plan prior to diabetic macular edema diagnosis, any history of proliferative retinopathy or any treatment that is used for diabetic macular edema. Covariates of interest were demographic characteristics, laboratory values, and clinical factors such as previous anti-vascular endothelial growth factor used, number of involved eyes, year of treatment, and time since last injection. Those variables that changed with time were assessed and updated at each visit. The main outcome measure was the odds of receiving treatment at any visit. Results: In total, 189 new diabetic macular edema patients with follow-up were analyzed, covering 729 visits with 543 (74.5%) receiving treatment. Univariate analysis showed that male gender (odds ratio: 0.54, 95% confidence interval: 0.32–0.91, p = 0.03), every week since last injection (odds ratio: 0.94, 95% confidence interval: 0.91–0.97, p = 0.001), and having two eyes affected (odds ratio: 2.09, 95% confidence interval: 1.10–3.97, p = 0.02) were associated with getting an injection. After multivariate analysis, only time since previous injection with every week that passed reduced the odds on having an injection at the next visit (odds ratio: 0.95, 95% confidence interval: 0.92–0.97, p < 0.001). Anemia was not associated with receiving an injection (odds ratio: 1.05, 95% confidence interval: 0.61–1.80, p = 0.86). Conclusion: This study used time-varying methodology to better identify which patients will likely need an injection at any one visit. While anemia was not found to impact injections, our results can aid future endeavors that may incorporate clinical visit information in developing a full prediction model to help make diabetic macular edema care more efficient.

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Welsh, David A., Benoit P. H. Guery, Bennett P. Deboisblanc, Elizabeth P. Dobard, Colette Creusy, Donald Mercante, Steve Nelson, Warren R. Summer, and Carol M. Mason. "Keratinocyte growth factor attenuates hydrostatic pulmonary edema in an isolated, perfused rat lung model." American Journal of Physiology-Heart and Circulatory Physiology 280, no. 3 (March 1, 2001): H1311—H1317. http://dx.doi.org/10.1152/ajpheart.2001.280.3.h1311.

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Hydrostatic pulmonary edema is a common complication of congestive heart failure, resulting in substantial morbidity and mortality. Keratinocyte growth factor (KGF) is a mitogen for type II alveolar epithelial and microvascular cells. We utilized the isolated perfused rat lung model to produce hydrostatic pulmonary edema by varying the left atrial and pulmonary capillary pressure. Pretreatment with KGF attenuated hydrostatic edema formation. This was demonstrated by lower wet-to-dry lung weight ratios, histological evidence of less alveolar edema formation, and reduced alveolar accumulation of intravascularly administered FITC-labeled large-molecular-weight dextran in rats pretreated with KGF. Thus KGF attenuates injury in this ex vivo model of hydrostatic pulmonary edema via mechanisms that prevent increases in alveolar-capillary permeability.

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Bastarache, Julie A., Ling Wang, Zhengming Wang, Kurt H. Albertine, Michael A. Matthay, and Lorraine B. Ware. "Intra-alveolar tissue factor pathway inhibitor is not sufficient to block tissue factor procoagulant activity." American Journal of Physiology-Lung Cellular and Molecular Physiology 294, no. 5 (May 2008): L874—L881. http://dx.doi.org/10.1152/ajplung.00372.2007.

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The alveolar compartment in acute lung injury contains high levels of tissue factor (TF) procoagulant activity favoring fibrin deposition. We previously reported that the alveolar epithelium can release TF procoagulant activity in response to a proinflammatory stimulus. To test the hypothesis that the alveolar epithelium further modulates intra-alveolar fibrin deposition through secretion of an endogenous inhibitor to TF, tissue factor pathway inhibitor (TFPI), we measured TFPI levels in edema fluid (EF) from patients with acute respiratory distress syndrome. To determine whether the alveolar epithelium can release TFPI, both full-length TFPI and truncated TFPI were measured (ELISA) in pulmonary edema fluid from patients with acute respiratory distress syndrome (ARDS) and a control group of patients with hydrostatic pulmonary edema (HYDRO). TFPI protein was also measured in conditioned media (CM) and cell lysates (CL) from human alveolar epithelial cells (A549) after exposure to cytomix (TNF-α, IL-1β, IFN-γ). TFPI protein levels were higher in pulmonary edema fluid from patients with ARDS vs. HYDRO. TFPI protein was increased in CM and did not change in CL after cytomix treatment; TFPI mRNA levels (RT-PCR) did not change. Despite the high levels of TFPI, both the EF and CM retained significant TF procoagulant activity as measured by plasma recalcification time. The majority of intra-alveolar TFPI was in a truncated, inactive form, whereas the majority of TFPI released from cells was full length, suggesting different mechanisms of inactivation. In summary, the alveolar epithelium releases TFPI in response to an inflammatory stimulus but does not increase TFPI gene transcription or protein production. Levels of intra-alveolar TFPI in ARDS are not sufficient to block intra-alveolar TF procoagulant activity due to truncation and inactivation of intra-alveolar TFPI.

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SONOKAWA, Tadao. "Effect of Hydrostatic Factor on Ischemic Brain Edema." Neurologia medico-chirurgica 28, no. 6 (1988): 538–45. http://dx.doi.org/10.2176/nmc.28.538.

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Kim, Yu-Gene. "Purification and Characterization of Recombinant Anthrax Edema Factor." Journal of the Korea Institute of Military Science and Technology 14, no. 4 (August 5, 2011): 710–18. http://dx.doi.org/10.9766/kimst.2011.14.4.710.

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Lally, David R., Chirag P. Shah, and Jeffrey S. Heier. "Vascular endothelial growth factor and diabetic macular edema." Survey of Ophthalmology 61, no. 6 (November 2016): 759–68. http://dx.doi.org/10.1016/j.survophthal.2016.03.010.

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Rose, Sandra, Shasha Wu, Anne Jiang, Jisoon Kim, and James X. Tao. "Neurogenic pulmonary edema: An etiological factor for SUDEP?" Epilepsy & Behavior 52 (November 2015): 76–77. http://dx.doi.org/10.1016/j.yebeh.2015.08.010.

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Tang, Wei-Jen, and Qing Guo. "The adenylyl cyclase activity of anthrax edema factor." Molecular Aspects of Medicine 30, no. 6 (December 2009): 423–30. http://dx.doi.org/10.1016/j.mam.2009.06.001.

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Pin, Y., M. Loo, W. Waissi, A. Paix, J. Todeschi, D. Antoni, F. Proust, G. Ahle, and G. Noël. "P13.13 Clinical factors involved in brain metastasis edema: results of a retrospective cohort and evaluation of the best edema descriptor." Neuro-Oncology 21, Supplement_3 (August 2019): iii65. http://dx.doi.org/10.1093/neuonc/noz126.234.

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Abstract BACKGROUND Brain metastasis (BM) are frequently surrounded by brain edema with a variable extension. This pathological increase in the water mass from the interstitial or intracellular space is the source of neurological symptoms but some studies also showed a prognosis impact of this edema. Nevertheless, the current edema evaluation methods are poorly reproducible and were not extensively evaluated. From a series of patients with brain metastasis, we analyzed factors influencing perilesional edema extension in function of three edema descriptors which were qualitatively evaluated: the absolute cumulative intracranial edema volume (CIEV, in mL), the edema on tumor volume ratio (ER), and the Edema Theoretical Thickness (ETT, in mm), new factor designed to be more independent from geometrical considerations. MATERIAL AND METHODS Clinical, biological and imaging factors were retrospectively recorded from patients referred for upfront stereotactic radiotherapy of one to three BMs. CIEV, ER and ETT were calculated for each patient. Non-colinear factors were selected using the Farrar-Glauber test. Impact of these factors on edema was tested with an univariate then a multivariate linear regression for each edema descriptor. Each resulting regression model was qualitatively evaluated using the F-test, R square value and residuals calculation. RESULTS Between January 2012 to December 2017, 182 patients were included. Upon 20 potentially prognostic factors recorded, 10 were kept, including clinical, biological and imaging factors. In the multivariate analysis, the CIEV was influenced by the cumulative intracranial tumor volume (CITV) (coefficient of 1.95, p<.001). The CIEV F-statistic p-value and R square were <10–15 and 0.30, respectively. The ETT was significantly influenced by the CITV (0.31, p<.001) and the extracerebral disease control (-1.58, p=.049). The F-test p-value and R square were <10-10 and 0.25, respectively. No significant linear regression was found for the ER. Residuals were more clinically relevant for the ETT compared to the CIEV. CONCLUSION Being significantly influenced by the cumulative brain tumor volume and the extracerebral disease control, the ETT might be a factor to include in future BM works because its strong relationships with confounding factors and its ability to provide robust intra and inter subjects comparisons.

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Moayeri, Mahtab, Devorah Crown, Guan-Sheng Jiao, Seongjin Kim, Alan Johnson, Clinton Leysath, and Stephen H. Leppla. "Small-Molecule Inhibitors of Lethal Factor Protease Activity Protect against Anthrax Infection." Antimicrobial Agents and Chemotherapy 57, no. 9 (June 17, 2013): 4139–45. http://dx.doi.org/10.1128/aac.00941-13.

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ABSTRACTBacillus anthracis, the causative agent of anthrax, manifests its pathogenesis through the action of two secreted toxins. The bipartite lethal and edema toxins, a combination of lethal factor or edema factor with the protein protective antigen, are important virulence factors for this bacterium. We previously developed small-molecule inhibitors of lethal factor proteolytic activity (LFIs) and demonstrated theirin vivoefficacy in a rat lethal toxin challenge model. In this work, we show that these LFIs protect against lethality caused by anthrax infection in mice when combined with subprotective doses of either antibiotics or neutralizing monoclonal antibodies that target edema factor. Significantly, these inhibitors provided protection against lethal infection when administered as a monotherapy. As little as two doses (10 mg/kg) administered at 2 h and 8 h after spore infection was sufficient to provide a significant survival benefit in infected mice. Administration of LFIs early in the infection was found to inhibit dissemination of vegetative bacteria to the organs in the first 32 h following infection. In addition, neutralizing antibodies against edema factor also inhibited bacterial dissemination with similar efficacy. Together, our findings confirm the important roles that both anthrax toxins play in establishing anthrax infection and demonstrate the potential for small-molecule therapeutics targeting these proteins.

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Kumar, Praveen, Nidhi Ahuja, and Rakesh Bhatnagar. "Anthrax Edema Toxin Requires Influx of Calcium for Inducing Cyclic AMP Toxicity in Target Cells." Infection and Immunity 70, no. 9 (September 2002): 4997–5007. http://dx.doi.org/10.1128/iai.70.9.4997-5007.2002.

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ABSTRACT The anthrax edema toxin comprises two proteins: protective antigen and edema factor. Anthrax protective antigen binds to the receptors on the surface of target cells and facilitates the entry of edema factor into these target cells. Edema factor (EF) is an adenylate cyclase that catalyzes the synthesis of cyclic AMP (cAMP) in the cytosol of the host cells. In this study, we examined the requirement of extracellular calcium for anthrax edema toxin-induced toxicity in host cells. The cAMP response generated by edema toxin was analyzed in a variety of cells, including CHO, macrophage-like RAW264.7, human neutrophils, and human lymphocytes. Our investigations reveal that after EF reaches the cell cytosol, a rapid influx of calcium is triggered in the host cell that has a pivotal role in determining the cAMP response of the affected cells. Although the cAMP response generated by edema toxin in different cell types varied in intensity and in the time of initiation, the influx of calcium invariably preceded cAMP accumulation. Agents that blocked the uptake of calcium also inhibited edema toxin-induced accumulation of cAMP in the host cells. This is the first report that demonstrates that edema toxin induces accumulation of cAMP in lymphocytes. By accumulating cAMP, a potent inhibitor of immune cell function, edema toxin may actually be poisoning the immune system and thus facilitating the survival of the bacteria in the host.

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Strugar, John, David Rothbart, William Harrington, and Gregory R. Criscuolo. "Vascular permeability factor in brain metastases: correlation with vasogenic brain edema and tumor angiogenesis." Journal of Neurosurgery 81, no. 4 (October 1994): 560–66. http://dx.doi.org/10.3171/jns.1994.81.4.0560.

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✓ Metastatic brain tumors are almost always associated with vasogenic brain edema, which in turn plays a pivotal role in the evolution of neurological morbidity associated with these lesions. Attention has recently focused on a group of proteinaceous vascular permeability factors (VPF's) that are capable of inducing angiogenesis and promoting increased capillary permeability. To test the hypothesis that metastatic brain tumors expressing VPF's are associated with peritumoral cerebral edema, a rabbit polyclonal immunoglobulin (Ig) G anti-VPF was used to immunostain pathological specimens of metastatic cerebral tumors obtained from 22 patients who underwent surgery at Yale-New Haven Hospital. Magnetic resonance (MR) imaging was used to correlate VPF staining in tumor tissue with the occurrence of peritumoral brain edema. A histological antigen, using two gliosis specimens as controls. Results revealed 21 of 22 tumors stained positively for VPF's; the negative-VPF tumor was a melanoma that exhibited no peritumoral edema. Twenty of 22 tumors had MR imaging-evident vasogenic edema. The presence and intensity of VPF immunostaining of microvascular features were noted and compared. Factor VIII staining demonstrated tumor vascularity to be most abundant in VPF-rich regions of tumor. The authors therefore report a high correlation between the presence of VPF's and the occurrence of peritumoral brain edema associated with cerebral metastases.

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Bartsch, P., B. Lammle, I. Huber, A. Haeberli, P. Vock, O. Oelz, and P. W. Straub. "Contact phase of blood coagulation is not activated in edema of high altitude." Journal of Applied Physiology 67, no. 4 (October 1, 1989): 1336–40. http://dx.doi.org/10.1152/jappl.1989.67.4.1336.

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To examine whether bradykinin generated by the activation of the contact phase of blood coagulation is involved in the pathogenesis of edema occurring after acute exposure to high altitude, 15 mountaineers were examined at 490 m and 1, 3, and 5 days after arrival at 4,559 m. The clotting activity levels of factor XII, factor XI, plasma prekallikrein, and high-molecular-weight kininogen (HMWK) were measured, and plasma kallikrein-induced proteolytic cleavage of HMWK was assessed by ligand blotting by use of radiolabeled factor XI. After an ascent on foot from 1,170 to 4,559 m in 3 days, three subjects developed high-altitude pulmonary edema, and four subjects presented facial edema. There was no evidence for activation of the contact system in any subject as demonstrated by the lack of proteolytic cleavage of HMWK at high altitude. The absence of contact system activation was further supported by stable plasma levels of the individual factors of contact activation. Therefore, we conclude that bradykinin generated by plasma kallikrein-induced cleavage of HMWK is not involved in the pathogenesis of edema due to acute exposure to high altitude.

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Abreu-Gonzalez, Rodrigo, Roberto Gallego-Pinazo, Maximino Abraldes, Isabel Pinilla, and María I. Lopez-Galvez. "Management of diabetic macular edema patients in clinical practice in Spain." European Journal of Ophthalmology 29, no. 6 (October 7, 2018): 664–72. http://dx.doi.org/10.1177/1120672118804079.

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Purpose: Diabetic macular edema is the main cause of blindness in diabetic patients. Vascular endothelial growth factor is involved in diabetic macular edema pathogenesis. Vascular endothelial growth factor inhibitors are an important option in diabetic macular edema therapy. This survey investigates actual clinical practice in diabetic macular edema in Spain. Methods: An expert advisory panel of 17 Spanish ophthalmologists developed a 30-item anonymous questionnaire about diagnosis, treatment, and follow-up in diabetic macular edema. A total of 137 ophthalmologists from 10 Spanish regions completed the questionnaire online. Results: Almost all of the respondents (99.3%) record the measured visual acuity and perform biomicroscopic anterior (94.9%) and posterior (91.2%) segment examinations. Similarly, 100% of responding ophthalmologists always/almost always or frequently perform optical coherence tomography. Most respondents (65%) always/almost always or frequently perform a retinography. More than 50% rarely perform fluorescein angiography. Nearly, all (96.4%) of the specialists responded that, in center-involved diabetic macular edema, the first treatment is an anti–vascular endothelial growth factor drug. For corticosteroids, the first choice of most respondents (91.2%) was the dexamethasone implant. In the follow-up, almost all (96.4%) specialists record the measured visual acuity and most also perform biomicroscopic anterior (82.5%) and posterior (83.2%) segment examination. Conclusion: This survey shows the actual clinical practice in diabetic macular edema in Spain, finding that anti–vascular endothelial growth factor therapy is frequently used, and that diagnosis, treatments, and follow-up examinations used by specialists are homogeneous and according to diabetic macular edema guidelines.

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Noma, Hidetaka, Kanako Yasuda, and Masahiko Shimura. "Cytokines and the Pathogenesis of Macular Edema in Branch Retinal Vein Occlusion." Journal of Ophthalmology 2019 (May 2, 2019): 1–9. http://dx.doi.org/10.1155/2019/5185128.

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Branch retinal vein occlusion (BRVO) is a very common retinal vascular problem in patients with lifestyle-related diseases, such as hypertension and arteriosclerosis. In patients with BRVO, development of macular edema is the main cause of visual impairment. BRVO is still a controversial condition in many respects. Over the years, various methods such as laser photocoagulation have been tried to treat macular edema associated with BRVO, but the results were not satisfactory. After vascular endothelial growth factor (VEGF) was found to have an important role in the pathogenesis of macular edema in BRVO patients, treatment of this condition was revolutionized by development of anti-VEGF therapy. Although macular edema improves dramatically following intraocular injection of anti-VEGF agents, repeated recurrence and resistance of edema is a major problem in some BRVO patients. This suggests that factors or cytokines other than VEGF may be associated with inflammation and retinal hypoxia in BRVO and that the pathogenesis of macular edema is complicated. The present review assesses the role of various factors and cytokines in the pathogenesis of macular edema associated with BRVO. We present a mechanism that is not only plausible but should also be useful for developing new therapeutic strategies.

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Pistoiesi, Sabina, Gabriella Fontanini, Laura Boldrini, Tiziano Camacci, Katia De leso, Giancarlo Lupi, Michele Caniglia, et al. "The Role of Somatostatin in Vasogenic Meningioma Associated Brain Edema." Tumori Journal 89, no. 2 (March 2003): 136–40. http://dx.doi.org/10.1177/030089160308900206.

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Many tumors, including meningiomas, express somatostatin receptors, suggesting the application of somatostatin analogues for therapy and diagnosis. Sixty percent of meningiomas are associated with perilesional edema, whose development seems to be related to the vascular endothelial growth factor, although it requires an efficient pial blood supply. However, in several neoplastic models, other mediators seem to cooperate with vascular endothelial growth factor in regulating angiogenesis. We evaluated somatostatin receptors (sst2) in relation to the possibility that somatostatin analogues may influence vascular endothelial growth factor production with reduction of edema. Of 35 studied meningiomas, 21 presented peritumoural edema. Vascular endothelial growth factor, microvascular density and pial blood supply were significantly related to the edema (P = 0.0001, P = 0.0001, P = 0.0005). Similarly, a relation was found between sst2 and microvascular density (r = 0.58, P <0.001) and between sst2 and vascular endothelial growth factor expression (P = 0.03). This suggests that somatostatin analogues may be relevant for the treatment of meningiomas.

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Chaudhary, Karishma, Mamta Tyagi, Smriti Gupta, Manvi Gupta, Yamini Verma, and Kanishka Yadav. "Presentation of acute pulmonary edema in severe pre-eclamptic pregnant women: a case report." International Journal of Reproduction, Contraception, Obstetrics and Gynecology 10, no. 9 (August 26, 2021): 3620. http://dx.doi.org/10.18203/2320-1770.ijrcog20213499.

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Pulmonary edema refers to an excessive accumulation of fluid in the pulmonary interstitial and alveolar spaces. It may occur in low risk pregnancies but one very important predisposing factor is association with pre-eclampsia. Acute pulmonary edema during pregnancy is very rare and occurs in 0.08% pregnancies. About 3% of severe pre-eclamptic patients develop acute pulmonary edema. Several risk factors have been identified: preeclampsia or eclampsia, use of tocolytic therapy, severe infection, cardiac disease, iatrogenic fluid overload, and multiple gestations. This case examines one such presentation and reviews some of the diagnostic possibilities.

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Wilson, Michael R., Michael E. Goddard, Kieran P. O'Dea, Sharmila Choudhury, and Masao Takata. "Differential roles of p55 and p75 tumor necrosis factor receptors on stretch-induced pulmonary edema in mice." American Journal of Physiology-Lung Cellular and Molecular Physiology 293, no. 1 (July 2007): L60—L68. http://dx.doi.org/10.1152/ajplung.00284.2006.

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Ventilator-induced lung injury plays a crucial role in the outcome of patients with acute lung injury. Previous studies have shown a role for the cytokine tumor necrosis factor-α (TNF) in stretch-induced alveolar neutrophil recruitment, but the involvement of TNF in stretch-induced pulmonary edema is unclear. We investigated the effects of TNF through its individual p55 and p75 receptors on early pulmonary edema formation during high stretch ventilation, before neutrophil infiltration. Anesthetized wild-type or TNF receptor single/double knockout mice were ventilated with high tidal volume (∼38 ml/kg) for 2 h or until they developed arterial hypotension. Pulmonary edema was assessed by physiological parameters including respiratory mechanics and blood gases, and by lavage fluid protein, lung wet:dry weight ratio, and lung permeability measurements using fluorescence-labeled albumin. High stretch ventilation in wild-type and TNF receptor double knockout animals induced similar pulmonary edema, and only 25–30% of mice completed the protocol. In contrast, the p55 receptor knockout mice were strongly protected from edema formation, with all animals completing the protocol. Myeloperoxidase assay indicated that this protective effect was not associated with decreased pulmonary neutrophil sequestration. The p75 receptor knockout mice, however, displayed increased susceptibility to edema formation, and no animals survived the full 2 h. These results demonstrate a novel role for TNF signaling (independent from its effects on neutrophil recruitment) specifically through the p55 receptor, in promoting high stretch-induced pulmonary edema, whereas p75 signaling may play an opposing role.

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Do, Jae Rock, Jong-Hyun Oh, Roy S. Chuck, and Choul Yong Park. "Transient Corneal Edema is a Predictive Factor for Pseudophakic Cystoid Macular Edema after Uncomplicated Cataract Surgery." Korean Journal of Ophthalmology 29, no. 1 (2015): 14. http://dx.doi.org/10.3341/kjo.2015.29.1.14.

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Stoklosa, Joan C., and Avraham I. Rivkind. "Tumor Necrosis Factor Causes Increased Pulmonary Permeability and Edema." American Review of Respiratory Disease 138, no. 5 (November 1988): 1359–60. http://dx.doi.org/10.1164/ajrccm/138.5.1359a.

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Luks, Andrew M. "A Novel Risk Factor for High Altitude Pulmonary Edema?" Wilderness & Environmental Medicine 25, no. 4 (December 2014): 490–92. http://dx.doi.org/10.1016/j.wem.2014.04.016.

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Winking, M., W. Deinsberger, A. Joedicke, and D. K. Boeker. "Cysteinyl-Leukotriene Levels in Intracerebral Hemorrhage:An Edema-Promoting Factor?" Cerebrovascular Diseases 8, no. 6 (1998): 318–26. http://dx.doi.org/10.1159/000015874.

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Pitard, Irène, Catherine Simenel, Damien Monet, Christophe Thomas, Peggy Suzanne, Arnaud Blondel, Jacques Bellalou, et al. "Edema Factor Of Bacillus Anthracis Interacting with its Inhibitors." Biophysical Journal 116, no. 3 (February 2019): 482a—483a. http://dx.doi.org/10.1016/j.bpj.2018.11.2606.

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Reilly, Eileen, and Justin Hwang. "Listeria Cerebritis with Tumor Necrosis Factor Inhibition." Case Reports in Infectious Diseases 2020 (April 25, 2020): 1–5. http://dx.doi.org/10.1155/2020/4901562.

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Background. Listeria monocytogenes is historically a central nervous system pathogen of consideration in the very young, very old, and immune suppressed. Diagnosis of Listeria is based on positive bodily fluid culture or PCR testing. Cerebral edema is nonspecific and can be a manifestation of vasculitis, trauma, anoxia, ischemia, infarction, malignancy, or an infectious process. A main mechanism of immune protection against Listeria is tumor necrosis factor (TNF). Lenalidomide, an immunosuppressant, inhibits TNF. Case Presentation. A 61-year-old female with diabetes mellitus 2 and multiple myeloma treated with stem cell transplant and immunosuppressant (lenalidomide) was found to have cerebral edema after presenting with headache for 3 weeks and new focal neurologic deficits. Vitals signs were stable, with no meningeal exam findings and unremarkable initial serum testing. Blood cultures on days 0 and 2 of hospitalization as well as cerebral spinal fluid cultures were negative for infectious organisms. PCR testing of CSF was also negative for microorganisms. Brain biopsy was scheduled but postponed due to outstanding prion testing. The patient’s focal neurologic deficits worsened prompting administration of dexamethasone after extensive negative infectious disease workup. By day 6, gross neurologic function deteriorated prompting transfer to higher level of care where the patient spiked a fever and one set of blood cultures revealed Gram-positive bacillus. Aggressive antimicrobial therapy was initiated, excluding ampicillin; however, this was later added. Blood culture further identified Listeria monocytogenes. By day 17, the patient suffered demise. Autopsy revealed brain microabscess lesions consistent with Listeria. Conclusion. Clinicians should employ prophylactic antimicrobial treatment for Listeria when caring for those patients presenting with cerebral edema who are immune suppressed with TNF inhibition no matter the initial exam findings, serum testing, and/or radiologic interpretation. If initial workup is negative and brain biopsy is needed to determine the next course of action in the patient with cerebral edema, transfer the patient to a higher level of care if unable to complete biopsy at your facility in an expedient fashion.

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Sansing, Lauren H., Elena A. Kaznatcheeva, Candice J. Perkins, Eugene Komaroff, Frederick B. Gutman, and George C. Newman. "Edema after intracerebral hemorrhage: correlations with coagulation parameters and treatment." Journal of Neurosurgery 98, no. 5 (May 2003): 985–92. http://dx.doi.org/10.3171/jns.2003.98.5.0985.

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Object. Development of edema is known to contribute to poor outcome after spontaneous intracerebral hemorrhage (ICH). Recent research has identified thrombin as a key mediator in the development of edema in animal models; however, little has been published correlating the coagulation cascade and edema in humans. Methods. In this retrospective clinical study of 80 patients with spontaneous supratentorial ICH, the authors sought to identify factors associated with edema development and outcome, including lesion imaging parameters, anticoagulant use, international normalized ratio and platelet count on hospital admission, and treatment with mannitol and steroid medications. A multivariate model was used to identify edema volume, use of mannitol, elevated blood glucose, and the presence of intraventricular hemorrhage as predictors of poor outcome at the time patients were discharged from the hospital. The authors developed a quadratic model for predicting edema volume against time by using a random coefficients model, and found that edema peaks between Days 5 and 6 after onset of ICH. The volume of the hemorrhage and the platelet count correlated significantly with edema volume within the first 24 hours post-ICH in the multiple regression analysis (p < 0.0001, r2 = 0.75). Edema growth during the first 5 days post-ICH also correlated with the platelet count, with an increasing platelet count associated with an increasing growth of edema (p = 0.0013). Conclusions. The authors propose that factors released from activated platelets at the site of hemorrhage, for example vascular endothelial growth factor, may interact with thrombin to increase vascular permeability and contribute to the development of edema.

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Gordon, T., and D. Sheppard. "Tumor necrosis factor inhibits a polymorphonuclear leukocyte-dependent airway edema in guinea pigs." Journal of Applied Physiology 64, no. 4 (April 1, 1988): 1688–92. http://dx.doi.org/10.1152/jappl.1988.64.4.1688.

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Intravenously administered endotoxin inhibits the polymorphonuclear leukocyte (PMN)-dependent airway edema produced in guinea pigs exposed to toluene diisocyanate (TDI). Tumor necrosis factor (TNF) is produced in vivo by peripheral blood monocytes and tissue macrophages stimulated with endotoxin and has been shown to activate PMN's and vascular endothelial cells. To determine whether the inhibition of airway edema is mediated by TNF, guinea pigs were treated with intravenous saline or 75,000 U/kg recombinant human TNF 1.5 h before exposure to air or 3 ppm TDI for 1 h. Animals were then injected intravenously with 50 mg/kg Evans blue dye as a marker of protein extravasation. Saline-treated animals exposed to TDI had a significant increase in tracheal Evans blue dye extravasation (85 +/- 6.5 micrograms dye/g trachea, mean +/- SE) compared with saline-treated animals exposed to air (31.3 +/- 2.5, P less than 0.001). The tracheal extravasation of Evans blue dye was significantly inhibited (P less than 0.05) in TDI-exposed animals treated with TNF (64.7 +/- 7.5). Neither heat-inactivated TNF (104.9 +/- 9.5) nor TNF neutralized with a monoclonal antibody against TNF (99.7 +/- 17.9) inhibited TDI-induced airway edema. In addition, treatment with 15,000 U/kg (99.9 +/- 21.3) or 150,000 U/kg (103.2 +/- 17.6) interleukin 1, a monokine also produced in response to endotoxin, did not prevent airway edema. These results suggest that TNF released in response to endotoxin mediates endotoxin's inhibition of a PMN-dependent airway edema.

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Chauhan, Muhammad Z., Peyton A. Rather, Sajida M. Samarah, Abdelrahman M. Elhusseiny, and Ahmed B. Sallam. "Current and Novel Therapeutic Approaches for Treatment of Diabetic Macular Edema." Cells 11, no. 12 (June 17, 2022): 1950. http://dx.doi.org/10.3390/cells11121950.

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Diabetic macular edema (DME) is a major ocular complication of diabetes mellitus (DM), leading to significant visual impairment. DME’s pathogenesis is multifactorial. Focal edema tends to occur when primary metabolic abnormalities lead to a persistent hyperglycemic state, causing the development of microaneurysms, often with extravascular lipoprotein in a circinate pattern around the focal leakage. On the other hand, diffusion edema is due to a generalized breakdown of the inner blood–retinal barrier, leading to profuse early leakage from the entire capillary bed of the posterior pole with the subsequent extravasation of fluid into the extracellular space. The pathogenesis of DME occurs through the interaction of multiple molecular mediators, including the overexpression of several growth factors, including vascular endothelial growth factor (VEGF), insulin-like growth factor-1, angiopoietin-1, and -2, stromal-derived factor-1, fibroblast growth factor-2, and tumor necrosis factor. Synergistically, these growth factors mediate angiogenesis, protease production, endothelial cell proliferation, and migration. Treatment for DME generally involves primary management of DM, laser photocoagulation, and pharmacotherapeutics targeting mediators, namely, the anti-VEGF pathway. The emergence of anti-VEGF therapies has resulted in significant clinical improvements compared to laser therapy alone. However, multiple factors influencing the visual outcome after anti-VEGF treatment and the presence of anti-VEGF non-responders have necessitated the development of new pharmacotherapies. In this review, we explore the pathophysiology of DME and current management strategies. In addition, we provide a comprehensive analysis of emerging therapeutic approaches to the treatment of DME.

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Carter, Eric A., and Michael S. Koehle. "Immersion Pulmonary Edema in Female Triathletes." Pulmonary Medicine 2011 (2011): 1–4. http://dx.doi.org/10.1155/2011/261404.

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Pulmonary edema has been reported in SCUBA divers, apnea divers, and long-distance swimmers however, no instances of pulmonary edema in triathletes exist in the scientific literature. Pulmonary edema may cause seizures and loss of consciousness which in a water environment may become life threatening. This paper describes pulmonary edema in three female triathletes. Signs and symptoms including cough, fatigue, dyspnea, haemoptysis, and rales may occur within minutes of immersion. Contributing factors include hemodynamic changes due to water immersion, cold exposure, and exertion which elevate cardiac output, causing pulmonary capillary stress failure, resulting in extravasation of fluid into the airspace of the lung. Previous history is a major risk factor. Treatment involves immediate removal from immersion and in more serious cases, hospitalization, and oxygen administration. Immersion pulmonary edema is a critical environmental illness of which triathletes, race organizers, and medical staff, should be made aware.

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Bormann, Caroline, Jens Heichel, Ute Hammer, Anke Habermann, and Thomas Hammer. "Intravitreal Anti-Vascular Endothelial Growth Factor for Macular Edema due to Complex Retinal Arterial Macroaneurysms." Case Reports in Ophthalmology 8, no. 1 (March 7, 2017): 141–47. http://dx.doi.org/10.1159/000458517.

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Introduction: Complex retinal arterial macroaneurysms (RAM) are often accompanied by hemorrhage and/or affect the macula. We evaluated the effect of intravitreal anti-vascular endothelial growth factor (anti-VEGF) therapy using ranibizumab or aflibercept with or without laser photocoagulation in the treatment of macular edema due to RAM. Methods: A case report of two patients with secondary macular edema caused by RAM is presented. The first case was a 76-year-old female treated with two 0.5-mg injections of ranibizumab and additional focal laser photocoagulation. This patient presented a solely intraretinal exudation. The second patient was a 96-year-old female, who received one 2.0-mg injection of aflibercept. She showed sub- and intraretinal edema. We documented the clinical courses of these patients based on fundus photography, fluorescein angiography, and spectral-domain optical coherence tomography. Patients were followed-up for 12 months. Results: Patients were treated successfully using anti-VEGF therapy (ranibizumab or aflibercept) with or without laser photocoagulation. In both cases, we observed a complete regression of the macular edema and an increase in visual acuity. Conclusion: RAM can manifest with heterogeneous findings. Intravitreal anti-VEGF therapy with or without laser photocoagulation may be an effective treatment option in cases of macular edema due to RAM. Aflibercept and ranibizumab seem to be a potent anti-VEGF therapy for RAM. Individualized patient care is needed.

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Hocking, D., T. J. Ferro, and A. Johnson. "Dextran sulfate and heparin sulfate inhibit platelet-activating factor-induced pulmonary edema." Journal of Applied Physiology 72, no. 1 (January 1, 1992): 179–85. http://dx.doi.org/10.1152/jappl.1992.72.1.179.

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We tested the hypothesis that dextran sulfate and heparin sulfate inhibit platelet-activating factor- (PAF) induced pulmonary edema in the isolated perfused guinea pig lung via a charge-dependent mechanism. Dextran sulfate prevented the changes in pulmonary capillary pressure (Ppc, 7.8 +/- 0.9 vs. 14.0 +/- 0.7 cmH2O), lung weight gain (dW, +0.48 +/- 0.29 vs. +8.41 +/- 2.07 g), and pulmonary edema formation or wet-to-dry weight ratio [(W-D)/D, 6.5 +/- 0.3 vs. 13.2 +/- 2.6] occurring 60 min after PAF infusion (10(-11) M) into an isolated lung. The unsulfated form of dextran had no protective effect [Ppc, dW, and (W-D)/D, 11.9 +/- 1.4 cmH2O, +5.33 +/- 2.18 g, and 11.2 +/- 3.2, respectively]. The unrelated anionic compound, heparin sulfate, also inhibited the PAF response [Ppc, dW, and (W-D)/D, 7.0 +/- 0.5 cmH2O, +0.61 +/- 0.32 g, and 6.1 +/- 0.2, respectively], whereas the partially desulfated form of heparin was not effective in inhibiting PAF-induced edema [Ppc, dW, and (W-D)/D, 15.1 +/- 0.7 cmH2O, +6.07 +/- 1.58 g, and 10.0 +/- 1.2, respectively]. When the metachromatic dye crystal violet was used as an indicator of charge interactions, the sulfated compounds interacted with PAF in vitro. The data indicate that PAF-induced pulmonary edema is inhibited by sulfated polysaccharides, possibly via a charge interaction between negatively charged compounds and PAF.

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Islamova, L. I., and S. H. Aminev. "Anti-VEGF therapy of macular edema." POINT OF VIEW. EAST – WEST, no. 1 (May 3, 2023): 49–55. http://dx.doi.org/10.25276/2410-1257-2023-1-49-55.

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The development of macular edema in neovascular age-related macular degeneration, diabetic retinopathy, retinal vein occlusion and in many other diseases, often causes significant visual deterioration and blindness, including in people of working age. One of the methods used of treating these diseases is the intravitreal administration of anti-VEGF drugs, including ranibizumab, aflibercept, brolucizumab, etc. Faricimab is a new drug that affects both vascular endothelial growth factor and angiopoietins. In order to reduce the frequency of intravitreal injections and prolong the time of the drug effect, sustained-release devices have been developed: Port Delivery System and biodegradable drugs. Keywords: diseases of the retina, macular edema, vascular endothelial growth factor, angiopoietins, anti-VEGF drugs

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Yao, Wanzhen, Yanjing Zhang, Li Zhang, Jing Zhou, Yi Zhang, Xiaozhong Zheng, and Jianping Ding. "MRI features of and factors related to ankle injuries in asymptomatic amateur marathon runners." Skeletal Radiology 50, no. 1 (July 6, 2020): 87–95. http://dx.doi.org/10.1007/s00256-020-03530-9.

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Abstract Objective To analyze the MRI manifestations of and factors related to ankle injuries in asymptomatic amateur marathon runners. Materials and methods A total of 113 amateur marathon runners without any ankle joint symptoms were recruited. Each participant was asked to complete a questionnaire at the beginning of the study and underwent MRI of the ankle. The MRI manifestations of ankle injuries were summarized, and binary logistic regression analysis was applied to analyze the factors related to ankle injuries. Results The main MRI features were bone marrow edema-like signal intensity, peritendinous effusion, and partial lateral collateral ligament injury. Others included Achilles tendinopathy, cyst-like lesions, osteochondral lesions, and subcutaneous soft tissue edema. The risk factor for bone marrow edema-like signal intensity in amateur marathon runners was a rearfoot strike pattern (p = 0.028, OR = 1.172); the risk factors for peritendinous effusion were a higher weekly running distance (p = 0.013, OR = 1.685) and increased running years (p = 0.039, OR = 1.113), whereas a rearfoot strike pattern (p = 0.005, OR = 0.831) was a protective factor for peritendinous effusion; the risk factor for Achilles tendinopathy was increased age (p = 0.008, OR = 1.412); the risk factors for anterior talofibular ligament injury were a rearfoot strike pattern (p = 0.017, OR = 1.346) and higher weekly running distance (p = 0.022, OR = 1.171); and the factors for calcaneofibular ligament injury were a higher weekly running distance (p = 0.029, OR = 1.570) and rearfoot strike pattern (p = 0.035, OR = 1.463). Conclusion The main MRI features of asymptomatic amateur marathon runners are bone marrow edema-like signal intensity, peritendinous effusion, and partial lateral collateral ligament injury. In addition, increased age, increased running years, higher weekly running distance, and different foot strike patterns are risk factors for ankle injuries.

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Castro-Navarro, Verónica, Enrique Cervera-Taulet, Catalina Navarro-Palop, Laura Hernández-Bel, Clara Monferrer-Adsuara, Lucía Mata-Moret, and Javier Montero-Hernández. "Analysis of anatomical biomarkers in subtypes of diabetic macular edema refractory to anti-vascular endothelial growth factor treated with dexamethasone implant." European Journal of Ophthalmology 30, no. 4 (March 4, 2019): 764–69. http://dx.doi.org/10.1177/1120672119834182.

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Introduction: To analyze functional and anatomical outcomes in subtypes of diabetic macular edema treated with a single dexamethasone implant and to assess the usefulness of a pro-re-nata treatment among subtypes. Methods: Retrospective study in morphologic patterns of diabetic macular edema (diffuse retinal thickening n = 15; cystoid macular edema n = 38, and serous retinal detachment n = 17) recalcitrant to anti-vascular endothelial growth factor, treated with dexamethasone implant. Examinations included timing to recidive of diabetic macular edema, best-corrected visual acuity, and central subfield macular thickness at 2, 4, and 6 months. Results: In previously treated patients with a mean of 6.64 ± 3.69 anti-vascular endothelial growth factor injections, the best-corrected visual acuity improved from 61.64 ± 13.71 to 65.71 ± 14.65 as per the Early Treatment Diabetic Retinopathy Study protocol (p = 0.009) and central subfield macular thickness change from 447.46 ± 110.82 to 354.39 ± 80.46 µm (p < 0.005). The best-corrected visual acuity improvement was better in the diffuse retinal thickening group (68.67 ± 13.81 vs 65.26 ± 14.04 in cystoid macular edema and vs 64.12 ± 17.06 in serous retinal detachment), whereas higher central subfield macular thickness thinning was observed in serous retinal detachment group (368.47 ± 29.96 to 310.27 ± 67.47 in diffuse retinal thickening, vs 445.92 ± 105.06 to 364.39 ± 80.28 and 520.59 ± 122.96 to 370.94 ± 81.73 in cystoid macular edema and serous retinal detachment, respectively). Cystoid macular edema group was the group with more recurrences after 6 months (86.8% vs 66.7% in diffuse retinal thickening and 70.6% in serous retinal detachment). Conclusion: Dexamethasone implant is effective for all persistent diabetic macular edema subtypes with sustained functional and morphologic gains in the first 6 months.

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Zhao, Jingyan, Stephanie A. Roy, and Donald J. Nelson. "MD Simulations of Anthrax Edema Factor: Calmodulin Complexes with Mutations in the Edema Factor “Switch A” Region and Docking of 3′-deoxy ATP into the Adenylyl Cyclase Active Site of Wild-Type and Mutant Edema Factor Variants." Journal of Biomolecular Structure and Dynamics 21, no. 2 (October 2003): 159–70. http://dx.doi.org/10.1080/07391102.2003.10506914.

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Tessier, Emilie, Laurence Cheutin, Annabelle Garnier, Clarisse Vigne, Jean-Nicolas Tournier, and Clémence Rougeaux. "Early Circulating Edema Factor in Inhalational Anthrax Infection: Does It Matter?" Microorganisms 12, no. 2 (January 31, 2024): 308. http://dx.doi.org/10.3390/microorganisms12020308.

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Anthrax toxins are critical virulence factors of Bacillus anthracis and Bacillus cereus strains that cause anthrax-like disease, composed of a common binding factor, the protective antigen (PA), and two enzymatic proteins, lethal factor (LF) and edema factor (EF). While PA is required for endocytosis and activity of EF and LF, several studies showed that these enzymatic factors disseminate within the body in the absence of PA after intranasal infection. In an effort to understand the impact of EF in the absence of PA, we used a fluorescent EF chimera to facilitate the study of endocytosis in different cell lines. Unexpectedly, EF was found inside cells in the absence of PA and showed a pole-dependent endocytosis. However, looking at enzymatic activity, PA was still required for EF to induce an increase in intracellular cAMP levels. Interestingly, the sequential delivery of EF and then PA rescued the rise in cAMP levels, indicating that PA and EF may functionally associate during intracellular trafficking, as well as it did at the cell surface. Our data shed new light on EF trafficking and the potential location of PA and EF association for optimal cytosolic delivery.

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Noma, Hidetaka, Tatsuya Mimura, Kanako Yasuda, Hayate Nakagawa, Ryosuke Motohashi, Osamu Kotake, and Masahiko Shimura. "Intravitreal Ranibizumab and Aqueous Humor Factors/Cytokines in Major and Macular Branch Retinal Vein Occlusion." Ophthalmologica 235, no. 4 (2016): 203–7. http://dx.doi.org/10.1159/000444923.

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Aqueous humor levels of cytokines and growth/inflammatory factors were measured in 38 patients with macular edema who had major branch retinal vein occlusion (BRVO) or macular BRVO and were treated with intravitreal ranibizumab injection (IRI). Patients with recurrence of macular edema received further IRI as needed. Aqueous humor levels of vascular endothelial growth factor (VEGF), soluble VEGF receptor-1 (sVEGFR-1), and other cytokines/factors were measured. Compared with major BRVO, macular BRVO was associated with lower aqueous humor levels of sVEGFR-1, its ligands (VEGF and placental growth factor), and other growth/inflammatory factors (platelet-derived growth factor-AA, monocyte chemotactic protein-1, soluble intercellular adhesion molecule-1, interleukin-6, and interleukin-8). The mean number of IRI over 6 months was significantly lower in the macular BRVO group than in the major BRVO group. These findings suggest that macular BRVO requires fewer IRI than major BRVO and is associated with lower aqueous humor levels of various growth/inflammatory factors and cytokines.

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Kandatsu, Nobuhisa, Yong-Shan Nan, Guo-Gang Feng, Kimitoshi Nishiwaki, Mitsuru Hirokawa, Kiyonori Ishikawa, Toru Komatsu, Takashi Yokochi, Yasuhiro Shimada, and Naohisa Ishikawa. "Opposing Effects of Isoflurane and Sevoflurane on Neurogenic Pulmonary Edema Development in an Animal Model." Anesthesiology 102, no. 6 (June 1, 2005): 1182–89. http://dx.doi.org/10.1097/00000542-200506000-00018.

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Background The current study was undertaken to investigate the effects of pretreatment with isoflurane and sevoflurane on the development of neurogenic pulmonary edema in an animal model. Methods Rats were exposed to room air (control), 1.5% isoflurane, or 2.5% sevoflurane for 4 h. They were then anesthetized with intraperitoneal injections of pentobarbital sodium, and fibrinogen and thrombin were injected into the cisterna magna to induce neurogenic pulmonary edema. Results Consecutive injections of fibrinogen and thrombin caused increases in blood pressure, with the peak values obtained in the isoflurane and sevoflurane groups being lower than the control values. The incidence of significant neurogenic pulmonary edema was 58%, 100%, and 8% in the control, isoflurane, and sevoflurane groups, respectively. The lung water ratio, an index of severity of edema, was 4.86 +/- 0.78, 6.15 +/- 0.64, and 4.40 +/- 0.32 in the control, isoflurane, and sevoflurane groups, respectively. Furthermore, immunohistochemical staining for vascular endothelial growth factor demonstrated an increase of expression in the rat lungs exposed to isoflurane. Treatment with an anti-vascular endothelial growth factor antibody during exposure to isoflurane completely inhibited the effect of isoflurane to promote neurogenic pulmonary edema in this model. Conclusion Exposure to 1.5% isoflurane enhances the development of neurogenic pulmonary edema development in this animal model, most likely via release of vascular endothelial growth factor from bronchial epithelial cells, an effect not observed with sevoflurane.

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Pessoa, Bernardete, João Coelho, Constança Coelho, Sílvia Monteiro, Carolina Abreu, João Figueira, Angelina Meireles, and João Nuno Melo Beirão. "Enzymatic vitreolysis for the treatment of tractional diabetic macular edema." Therapeutic Advances in Ophthalmology 11 (January 2019): 251584141986951. http://dx.doi.org/10.1177/2515841419869511.

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Background: A new approach to address focal vitreomacular adhesion in patients with diabetic macular edema may control and stabilize diabetic macular edema with fewer anti-vascular endothelial growth factor injections. Objectives: The aim of this study was to demonstrate that diabetic macular edema can be improved by inducing the release of a vitreomacular adhesion, with less than 2500 μm, with enzymatic vitreolysis. Methods: From a retrospective analysis of clinical records from patients with diabetic retinopathy, patients with diabetic macular edema and vitreomacular adhesion <2500 μm were selected for a single-arm prospective study. The primary endpoint was to control diabetic macular edema with fewer anti-vascular endothelial growth factor injections after an observed vitreomacular adhesion release. A statistical subanalysis was performed for the following two groups: the group with vitreomacular adhesion release (group 1) and the group without vitreomacular adhesion release (group 2). Results: A total of 23 eyes from 19 patients were included. A reduction of the median number of injections was achieved in group 1 ( p = 0.006). Adverse events were mild and transitory. Conclusion: Release of vitreomacular adhesion <2500 μm through enzymatic vitreolysis contributed to the control and stabilization of diabetic macular edema with fewer anti-vascular endothelial growth factor injections, reducing the burden and the risks related to these invasive and frequently chronic treatments.

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Journal articles on the topic 'Edema factor'

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