Relevant bibliographies by topics / Oedema

Academic literature on the topic 'Oedema'

Author: Grafiati
Published: 4 June 2021
Last updated: 4 March 2023

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Journal articles on the topic "Oedema"

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King, Brenda. "Oedema, lymphovenous oedema and lymphoedema." Primary Health Care 16, no. 8 (October 25, 2006): 31–38. http://dx.doi.org/10.7748/phc.16.8.31.s5.

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Munnoch, Alex. "Chronic Oedema." British Journal of Community Nursing 17, Sup10 (October 2012): S3. http://dx.doi.org/10.12968/bjcn.2012.17.sup10.s3.

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Tufts, Mary H. "Pulmonary Oedema." AJN, American Journal of Nursing 113, no. 2 (February 2013): 66. http://dx.doi.org/10.1097/01.naj.0000426694.03955.62.

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Andrews, P. J. D. "Brain oedema." European Journal of Anaesthesiology 15, Supplement 17 (January 1998): 11–12. http://dx.doi.org/10.1097/00003643-199801001-00009.

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Morrow-Barnes, Abby. "Pulmonary oedema." Nursing Standard 30, no. 40 (June 2016): 61–62. http://dx.doi.org/10.7748/ns.30.40.61.s46.

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Thompson, Monica. "Pulmonary oedema." Nursing Standard 31, no. 14 (November 30, 2016): 64–65. http://dx.doi.org/10.7748/ns.31.14.64.s46.

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Ljubojević Hadžavdić, Suzana, Anamaria Jović, Ayla Hadžavdić, and Dragana Ljubojević Grgec. "Vulvar oedema." Contact Dermatitis 78, no. 3 (February 12, 2018): 226–27. http://dx.doi.org/10.1111/cod.12905.

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Green, Tracy. "Chronic Oedema." British Journal of Community Nursing 20, Sup10 (October 2015): S5. http://dx.doi.org/10.12968/bjcn.2015.20.sup10.s5.

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Lawrence, Paula. "Chronic Oedema." British Journal of Community Nursing 21, Sup10 (October 2016): S5. http://dx.doi.org/10.12968/bjcn.2016.21.sup10.s5.

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Ehrlich, Stefan, Uwe Querfeld, and Ernst Pfeiffer. "Refeeding oedema." European Child & Adolescent Psychiatry 15, no. 4 (February 23, 2006): 241–43. http://dx.doi.org/10.1007/s00787-006-0528-5.

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Dissertations / Theses on the topic "Oedema"

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McCreesh, Brendan. "Early detection and monitoring of diabetic macular oedema." Thesis, University of Ulster, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.399085.

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Ockrim, Z. K. "Diabetic macular oedema : the role of steroids and VEGF." Thesis, University College London (University of London), 2009. http://discovery.ucl.ac.uk/16290/.

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Despite advances in controlling diabetes, diabetic macular oedema remains the leading cause of blind registration in the working population in England and Wales. The only proven effective treatment for diabetic macular oedema is laser photocoagulation. However this treatment has limited benefits since it reduces the chance of moderate visual loss by approximately 50% and is unlikely to improve visual acuity. Intravitreal steroids have been used in the treatment for diabetic macular oedema. Initial pilot studies suggest it can decrease retinal thickening and increase visual acuity in the long-term. Vascular endothelial growth factor is thought to play a critical role during the pathogenesis of diabetic macular oedema. The mechanism of action of both steroids and vascular endothelial growth factor on permeability has still to be fully elucidated. The aims of this thesis were to establish a reliable model of retinal microvascular endothelial cells and to characterise cellular changes following exposure to corticosteroids or vascular endothelial growth factor. Separate clinical work was aimed at evaluating the benefits of steroid treatment alone or combined with pars plana vitrectomy as a treatment of diabetic macular oedema. We also aimed to identify any prognostic indicators for treatment by both examining the morphological features of diabetic macular oedema observed on optical coherence tomography and by assaying the vascular endothelial growth factor concentration in the ocular fluids of eyes with diabetic macular oedema. Our results show that our retinal and brain microvascular endothelial cells were morphologically very similar; in particular with respect to the spatial localization of junctional proteins. Vascular endothelial growth factor led to an increase in the permeability and a decrease in the staining of the junctional proteins. By using signal transduction inhibitors, we showed that vascular endothelial growth factor-induced permeability and vascular endothelial growth factor-induced zonula occludens-1 loss occurred via different pathways suggesting that zonula occludens-1 loss was unlikely to be the downstream effector of vascular endothelial growth factor-induced permeability. Hydrocortisone leads to a decrease in permeability and an increase in the junctional expression of a number of tight junctional proteins. Both hydrocortisone and triamcinolone were able to inhibit vascular endothelial growth factor but not lysophosphatidic acid induced permeability suggesting that steroids are able to counteract the effects of certain but all vasoactive compounds. Overall our results suggested that steroids and VEGF lead to opposing effects on microvascular endothelial cells. Our randomized controlled trial showed that intravitreal triamcinolone was no more beneficial than laser photocoagulation for persistent diabetic macular oedema. A retrospective analysis of the morphological characteristics observed on Optical coherence tomography did not provide any characteristic that was prognostic of the outcome of intervention. Additionally, an exploratory case series of pars plana vitrectomy with 4 mg intravitreal triamcinolone was unable to show that combined treatment was of benefit in the long-term. Lastly the intraocular concentration of vascular endothelial growth factor was not predictive of the outcome of treatment.
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Spooner, Kimberly. "Anti-VEGH Therapy in the Treatment of Macular Oedema." Thesis, The University of Sydney, 2019. https://hdl.handle.net/2123/21696.

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Macular oedema is one of the most common causes of permanent vision loss in patients with age-related macular degeneration, diabetic retinopathy, and retinal vein occlusion. Anti-Vascular endothelial growth factor agents reduce macular oedema and improve vision in eyes with macular oedema associated with AMD, DR, and RVO. However, not all eyes with resolved macular oedema show satisfactory visual outcomes. Impairment of photoreceptors is primarily responsible for this vision loss. Damage to photoreceptors can be caused by subretinal haemorrhages and exudates. Furthermore, the involvement of the inner retina by impairment of bipolar and ganglion cells due to ischaemia is a significant contributor to vision loss. Despite anti-VEGF therapy, a proportion of patients may have persistent macular oedema. The aim of the work detailed in this thesis is to investigate a number of clinical challenges of anti-VEGF therapy for the treatment of macular oedema, including, burden of treatment on patients, the efficacy of long-term treatment, the development of macular atrophy and treatment resistance. The primary aim of this thesis is to assess the effect of switching therapy to aflibercept for persistent macular oedema, in cases of treatment resistance. Given the spectrum of therapies available to date for the management of macular oedema secondary to RVO, aflibercept was demonstrated to be an effective option in cases of treatment resistance to prior anti-VEGF treatment, and has also shown good long-term outcomes, although with persistent treatment. The present study based on a small cohort of patients indicated that good results on retinal anatomy and function can be accomplished with fewer injections. Large-scale studies are needed to extrapolate these promising results.
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Patel, Jignesh I. "The pathophysiology of diabetic macular oedema : a clinicopathological assessment." Thesis, University College London (University of London), 2008. http://discovery.ucl.ac.uk/1445927/.

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Diabetic macular oedema (DMO) is a devastating vision-threatening complication of diabetes mellitus. The broad aim of the thesis is to investigate the hypothesis that vitreomacular traction and growth factors are important contributors to the development of DMO. The contribution of vitreomacular traction was evaluated on the macular structural indices (foveal thickness and macular volume by Optical Coherence Tomography) and on functional effects (best corrected visual acuity) after 3-port pars plana vitrectomy (PPV) as part of clinical pilot studies with and without internal limiting membrane peels studies. The evaluation of growth factors in the vitreous, which was obtained at pars plana vitrectomy was performed using ELISA methods,. These vitreous samples from macular oedema patients (clinically graded as nonproliferative diabetic retinopathy NPDR) were compared to patients with full thickness macular holes (FTMH) and proliferative diabetic retinopathy (PDR). Lastly, using an immortalised rat retinal endothelial cell line, the effect of VEGF was explored to determine the molecular change at the junctional level. In the non-randomised pilot series of PPV, there was a significant improvement in the structural and functional indices at 12 months compared to baseline (p=0.037, p=0.01 respectively). However, in the pilot randomised and nonrandomised study including ILM peel, surgery provided little visual improvement despite structural benefit. These clinical studies of pars plana vitrectomy do suggest a role of vitreomacular traction in the development of macular oedema. Vitreal VEGF-A and HGF (angiogenic) concentrations were increased with a corresponding decrease in the angiostatic agents (soluble Flt-1 R antibody and PEDF). There were also changes in the angiopoietin 1 and 2 concentrations with significantly lower concentrations of angiopoietin 1 in macular oedema, suggesting a lower anti-permeability protective effect of angiopoietin 1. Haemodynamic (endothelin-1) and inflammatory (II-1 P) markers in the patients with macular oedema also demonstrated changes compared to control patients especially in endothelin-1 where there was a significant decrease in its concentration in the diabetic macular oedema. The effect of VEGF on cultured immortalised retinal endothelial cells (with primary rat endothelial culture acting as a comparison) did demonstrate that high concentrations of VEGF (100 ng/ml) could disrupt the organisation of tight junctions. These results demonstrate that the development of diabetic macular oedema is multifactorial with a range of physical (vitreomacular) and biochemical (cytokine) forces acting on and within the retina to produce leakage of fluid into the macula.
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Rocker, Graeme Martin. "Studies on adult respiratory distress syndrome." Thesis, University of Oxford, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.235866.

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King, Nathalie Ghislaine. "Investigations into the causes and prevention of oedema in coriander." Thesis, University of Birmingham, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.435405.

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Al-Kashi, Adam. "An investigation into mechanisms underlying neutrophil-mediated oedema in vivo." Thesis, Imperial College London, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.498010.

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Neutrophils play a crucial role in the acute immune response. Inflammatory stimuli recruit neutrophils into the tissues. Post-migratory neutrophils may then engage in pathogen killing and phagocytosis. Oedema-formation is associated with neutrophil transmigration, although evidence indicates that these are mechanistically distinct phenomena. Leukocyte-driven oedema is a feature of many inflammatory diseases including asthma, rheumatoid arthritis, and Crohn's disease, the mechanisms underlying neutrophil-mediated oedema are unclear.
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Banz, Kelly. "Calming the ocular storm : the effect of corticosteroids in inflammatory oedema." University of Western Australia. Faculty of Life and Physical Sciences, 2009. http://theses.library.uwa.edu.au/adt-WU2009.0093.

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The primary aim of this research is to test the therapeutic potential of certain new generation corticosteroid drugs in order to develop safe and effective treatment for eye diseases that result in oedema, or swelling. The rising incidence of diabetes and the ageing population of developed countries mean that the prevalence of uveitis, diabetic retinopathy and age related macular degeneration will rise. Often, oedema is one of the reasons for vision loss. Corticosteroids are often used to reduce inflammation. Inflammation is one of several sources of oedema. Glucocorticoids, a class of corticosteroids that have anti-inflammatory properties, are thus used to treat ocular oedema. There is an unmet need to support clinical experience of the efficacy of steroids for ocular inflammation and oedema with more substantial scientific evidence. None of the drugs under investigation, with the exceptions of dexamethasone and triamcinolone, have been used for any ocular therapeutic purpose before. This thesis investigates “repurposing” fludrocortisone to the ophthalmic area. 11-Desoxycorticosterone (11D) and Deoxycorticosterone (DCS), other potentially valuable mineralocorticoids, remain completely untested. Lastly, Kenacort ®, or triamcinolone acetonide (TCA), is only used off-label by ophthalmologists. Methods: In the first study, corticosteroids, and especially mineralocorticoids, were investigated for their treatment efficacy in experimental uveitis, or intraocular inflammation (using a model known as endotoxin induced uveitis). In the second study, endothelial cells from choroidal blood vessels in the back of the eye were used in vitro to study whether corticosteroids reduce paracellular (between cells) permeability. Lastly, since endophthalmitis due to frequent injections is a side effect of corticosteroid use, the pharmacokinetics of different size formulations of corticosteroids were studied in an effort to find a formula that would have a prolonged dwell time within the eye.
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Kane, Philip John. "Brain oedema : pathophysiological studies in a rodent model of intracerebral haematoma." Thesis, University of Newcastle Upon Tyne, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.308750.

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Bahrami, Bobak. "Anti-VEGF Treatment for Diabetic Macular Oedema: Clinical and Laboratory Insights." Thesis, The University of Sydney, 2018. http://hdl.handle.net/2123/18755.

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Diabetic retinopathy (DR) is a leading cause of vision impairment, characterised by vascular damage and neurodegeneration. Anti vascular endothelial growth factor (VEGF) drugs have revolutionised the management of the most common cause of vision impairment in DR, diabetic macular oedema (DMO). These drugs restore vision in DMO and induce regression of vascular changes in DR. Despite anti-VEGF therapy, a proportion of patients may have persistent DMO. The aim of the research presented in this thesis is to investigate the effect of switching therapy between two anti-VEGF drugs for persistent DMO and to assess the potential effects of anti-VEGF drugs in modulating neurodegeneration in DR through production of neurotrophic factors. In a prospective, single-arm, open-label clinical trial of patients with persistent DMO despite prior treatment with bevacizumab, there was a significant improvement in visual and anatomical outcomes when therapy was switched to aflibercept. Artifacts on automated optical coherence tomography calculations were increased in the presence of DMO. Peripheral ischaemia was associated with a poorer baseline vision and greater vision gain. Microperimetry outcomes correlated with objective and subjective vision outcomes. Diabetic conditions were simulated in vitro using ARPE-19 cell-line culture. There was downregulation of pigment epithelium derived factor (PEDF) expression in hypoxic states. In the absence of hypoxia, the addition of anti-VEGF drugs led to a significant downregulation of PEDF. Brain derived neurotrophic factor secretion was downregulated in high glucose states and upregulated in hypoxia. This thesis has addressed a number of key issues relating to persistent DMO, a management challenge with a poor evidence base. Further research is required into the identification of clinical and laboratory biomarkers to individualise pharmacotherapy and identify patients who may be poor and good responders to anti-VEGF therapy.
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Books on the topic "Oedema"

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Tiwary, Satyendra K., ed. Approach to Lower Limb Oedema. Singapore: Springer Singapore, 2022. http://dx.doi.org/10.1007/978-981-16-6206-5.

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McCreesh, Brendan Michael. Early detection and monitoring of diabetic macular oedema. [S.l: The Author], 2003.

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Ubolsakka, Chulee. Cardiovascular responses to external compression and peripheral oedema during rest and exercise in man: A role for a muscle mechanoreflex? Birmingham: University of Birmingham, 2001.

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Gábor, M. Experimentally-induced paw oedemas in mice. Budapest: Akadémiai Kiadó, 2007.

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Verdonk, H. P. M., ed. Oedeem en oedeemtherapie. Houten: Bohn Stafleu van Loghum, 2011. http://dx.doi.org/10.1007/978-90-313-8442-6.

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Evans, A. Ernest. Acenion Gwynfyd: Canllawiau Cynnal oedfa. (Aberystwyth): (Cyngor Llyfrau Cymraeg), 1987.

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Casley-Smith, J. R. High-protein oedemas and the benzo-pyrones: The causes, effects, incidence and treatment of high-protein oedemas, including lymphoedema, and how these are improved by the benzo-pyrones, including the coumarins and the flavonoids. Sydney: Lippincott, 1986.

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1931-, Roberts Brynley F., ed. Cynnal oedfa: Cyfrol o wasanaethau crefyddol, gweddïau ac emynau. Caernarfon: Gwasg Pantycelyn, 1993.

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Kyŏngyŏng ŭn sallimsari oeda: Kyŏngyŏng susang. Sŏul Tʻŭkpyŏlsi: Ilsinsa, 1986.

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Gyda'r ifanc: Deunydd cynnal oedfa i blant a phobl ifainc. Abertawe: T^y John Penry, 1985.

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Book chapters on the topic "Oedema"

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Miller, J. D. "Cerebral Oedema." In Care of the Critically Ill Patient, 983–90. London: Springer London, 1992. http://dx.doi.org/10.1007/978-1-4471-3400-8_58.

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Kelehan, Peter, and Paul Downey. "Villous Oedema." In Pathology of the Placenta, 153–55. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-97214-5_21.

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Alemanno, Fernando. "Cerebral Oedema." In Biochemistry for Anesthesiologists and Intensivists, 97–117. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-26721-6_9.

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Alegria-Barrero, Eduardo, and Miguel A. San-Martin. "Pulmonary Oedema." In Complications of Percutaneous Coronary Intervention, 131–36. London: Springer London, 2016. http://dx.doi.org/10.1007/978-1-4471-4959-0_16.

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Chinard, Francis P. "Pulmonary Oedema." In Advances in Physiological Research, 353–75. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4615-9492-5_20.

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Frank, M. M. "Hereditary angio-oedema." In Complement in Health and Disease, 229–43. Dordrecht: Springer Netherlands, 1993. http://dx.doi.org/10.1007/978-94-011-2214-6_8.

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Bährle-Rapp, Marina. "Ödem, auch: Oedema." In Springer Lexikon Kosmetik und Körperpflege, 384. Berlin, Heidelberg: Springer Berlin Heidelberg, 2007. http://dx.doi.org/10.1007/978-3-540-71095-0_7090.

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Sallam, Ahmed, and Abdallah A. Ellabban. "Diabetic macular oedema." In Practical Manual of Diabetic Retinopathy Management, 93–115. Chichester, UK: John Wiley & Sons, Ltd, 2017. http://dx.doi.org/10.1002/9781119058984.ch7.

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Rudra, T. "Lower Limb Oedema." In Geriatric Medicine, 115–24. London: Springer London, 1989. http://dx.doi.org/10.1007/978-1-4471-1646-2_9.

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Kuntz, Erwin, and Hans-Dieter Kuntz. "Oedema and ascites." In Hepatology, 255–90. Berlin, Heidelberg: Springer Berlin Heidelberg, 2002. http://dx.doi.org/10.1007/978-3-662-04680-7_16.

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Conference papers on the topic "Oedema"

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Bork, K., and G. Witzke. "LCNG-TEFM SUBSTITUTION WITH Cl-INACTIVATOR IN PATIENTS WITH HEREDITARY AND ACQUIRED Cl-INH DEFICIENCY AND LIFE-THREATENING ANGIOEDEMA." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644329.

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Patients with hereditary car acquired cl-inactivator (Cl-INH) deficiency suffer frcm repeated episodes of oedema of the skin and internal organs, which often constitute a threat to life (laryngeal, pulmonary and brain oedama). The treatment which is rapidly effective in the other, much more common, forms of angio-oedema (idiopathic, allergic or anaphylactoid, often associated with urticaria) has little or no effect in these cases. This applies particularly to treatment with antihistamin agents and corticosteroids. However, in patients with hereditary angiooedana (HAE) Danazol is effective for long-term prophylaxis and the substitution of Cl-INH for acute treatment. In isolated cases long-term prophylaxis, which is generally reliable, cannot be used because of intolerability reactions. Moreover, it is ineffective in the oedema of acquired Cl-INH deficiency.As other forms of therapy did not achieve the desired response, long-term substitution with a concentrate of Cl-inactivator (Behringwerke AG, Marburg) was carried out in 2 patients (H.W., 47 yrs, male, hereditary angiooedana, 9 siblings died from angiooedana; W.K., 55 yrs, male, professional truipeter, suffering from angiooedana of unknown origin for 5 years, without other underlying disorders). The initial values wereSubstitution was carried out according to the clinical symptoms. Patient H.W. required 500 U Cl-inactivator every 4th day and patient W.K. 1000-1500 U every 5th day until. During substitution therapy (which in pat. H.W. has so far been carried out for 8 months and in pat. W.K. for 6 months) there was a rise in Cl-INH and C4 with an almost total absence of clinical syirptans. No undesirable effects were observed.
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Kolev, P., S. Stoyanov, S. Vassileva, and S. Adamova. "Laryngeal oedema – infection, allergy, laryngopharyngeal reflux." In Abstract- und Posterband – 89. Jahresversammlung der Deutschen Gesellschaft für HNO-Heilkunde, Kopf- und Hals-Chirurgie e.V., Bonn – Forschung heute – Zukunft morgen. Georg Thieme Verlag KG, 2018. http://dx.doi.org/10.1055/s-0038-1639745.

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Sogaolu, Olumide M., Adeniran Fawole, Fatai Balogun, and Stanley Erazua. "Tocolytic Pulmonary Oedema In A Nigerian Woman." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a4610.

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Barnafi, Nicolás, Brian Gómez-Vargas, Wesley de Jesus Lourenco, Ruy Freitas Reis, Bernardo Marcelo Rocha, Marcelo Lobosco, Ricardo Ruiz-Baier, and Rodrigo Weber dos Santos. "A large-strain poroelastic model for myocardial oedema formation." In 10th Vienna Conference on Mathematical Modelling. ARGESIM Publisher Vienna, 2022. http://dx.doi.org/10.11128/arep.17.a17182.

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Murphy, Greg, Thomas McGrath, Claire Hanley, Darren Roche, Asad Salim, and Edna Roche. "P117 Acute haemorrhagic oedema of infancy: an important spot diagnosis." In Faculty of Paediatrics of the Royal College of Physicians of Ireland, 9th Europaediatrics Congress, 13–15 June, Dublin, Ireland 2019. BMJ Publishing Group Ltd and Royal College of Paediatrics and Child Health, 2019. http://dx.doi.org/10.1136/archdischild-2019-epa.472.

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O’Sullivan, Deirdre, Rincy Koshy, Declan Cody, and Billy Bourke. "P336 Hypoalbuminemia and oedema in a 4 month-old boy." In Faculty of Paediatrics of the Royal College of Physicians of Ireland, 9th Europaediatrics Congress, 13–15 June, Dublin, Ireland 2019. BMJ Publishing Group Ltd and Royal College of Paediatrics and Child Health, 2019. http://dx.doi.org/10.1136/archdischild-2019-epa.685.

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Tadiotto, Elisa, Sara Pieropan, Maddalena Maschio, Giulia Aiello, Giulia Melotti, Federica Martinis, Erica Giacomelli, and Giorgio Piacentini. "AB1060 BONE MARROW FOOT OEDEMA IN CHILDREN: THE ROLE OF VITAMIN D." In Annual European Congress of Rheumatology, EULAR 2019, Madrid, 12–15 June 2019. BMJ Publishing Group Ltd and European League Against Rheumatism, 2019. http://dx.doi.org/10.1136/annrheumdis-2019-eular.1078.

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O'Neill, D. P., T. Peng, and S. J. Payne. "The response of hepatocyte cell volume to hyperthermia and its role in oedema." In 2011 33rd Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 2011. http://dx.doi.org/10.1109/iembs.2011.6091069.

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Mason, Rebecca H., Sophie D. West, Victor Chong, and John R. Stradling. "Prevalence Of Obstructive Sleep Apnoea (OSA) In 70 Patients With Diabetic Macular Oedema (DME)." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a3689.

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Mahmutovic Persson, Irma, Anders Örbom, Per-Ola Önnervik, Karin Von Wachenfeldt, and Lars E. Olsson. "Imaging biomarkers of oedema and fibrosis in a rat model of Drug-Induced-ILD." In ERS International Congress 2018 abstracts. European Respiratory Society, 2018. http://dx.doi.org/10.1183/13993003.congress-2018.pa2958.

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