Готові списки джерел за темами / Neovascularisation / Статті в журналах
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Статті в журналах з теми "Neovascularisation"

Автор: Grafiati
Опубліковано: 4 червня 2021
Оновлено: 20 липня 2024

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1

Creton, D. "Neovascularisation." Phlebologie 37, no. 03 (May 2008): 134–41. http://dx.doi.org/10.1055/s-0037-1622223.

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SummaryThere are different causes of neovascularisation: vascular endothelial growth factor, inflammatory process, hypertrophy of pre-existant vessels (lymph node veins), haematomas revascularisation, and high difference in pressure. The latter 3 depend directly on the way the operation is performed hence on the surgeon.Concerning the primary varices patch saphenoplasty do not abolish neovascularisation. It is of first importance to perform a flush ligation only in case of incontinent terminal and pre-terminal valves. In that case an incision as small as possible must be carried out with minimal dissection and with tumescence to limit the bleeding and hematomas. When the terminal valve is competent it is better to choose endovascular technique.Concerning re-do it is mandatory to avoid useless re-do, the best choice is foam sclerotherapy. I am convinced that neovascularisation are produced by the complications which are induced by a large dissection. The barrier technique are, probably, not as useful as we was told 10 years ago. The lack of aggressiveness during the operation is certainly far more important: “Doing less in the groin to do better for the recurrence and re-recurrence”
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2

Holmgren, L. "Malignant Neovascularisation." European Journal of Ultrasound 6 (November 1997): S11. http://dx.doi.org/10.1016/s0929-8266(97)87215-1.

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3

Smith, R. "Neovascularisation again." British Journal of Ophthalmology 74, no. 6 (June 1, 1990): 323. http://dx.doi.org/10.1136/bjo.74.6.323.

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4

Badal, Josep, Luis Amselem, Ricardo Aleman, and Frederic Huste. "Anti–vascular Endothelial Growth Factor Therapy for Myopic Choroidal Neovascularisation." European Ophthalmic Review 07, no. 02 (2013): 84. http://dx.doi.org/10.17925/eor.2013.07.02.84.

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Pathological myopia represents the most common cause of choroidal neovascularisation in young patients. Its natural course has a devastating prognosis. Several treatments have been assessed, but photodynamic therapy is currently the only approved treatment for subfoveal choroidal neovascularisation related to pathological myopia. Anti-vascular endothelial growth factor therapy has demonstrated promising results in any form and localisation of choroidal neovascularisation, although there is an absence of data obtained from randomised clinical trials. The aim of this article is to compare different treatment options, combinations and retreatment criteria for the management of choroidal neovascularisation in eyes with high myopia.
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5

Imre, G. "Lactic acid neovascularisation." British Journal of Ophthalmology 75, no. 4 (April 1, 1991): 254. http://dx.doi.org/10.1136/bjo.75.4.254.

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6

Shehadeh, Mohammad M., Mohammad T. Akkawi, Vasilios F. Diakonis, Ammar A. Aghbar, and Abdelraheem Abu Shanab. "Extensive Corneal Neovascularisation Treatment by Ultraviolet Corneal Collagen Crosslinking." European Ophthalmic Review 11, no. 01 (2017): 62. http://dx.doi.org/10.17925/eor.2017.11.01.62.

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The purpose of this article is to report a case of extensive corneal neovascularisation that was treated by ultraviolet corneal collagen crosslinking (CXL). The case report is about a 24-year-old man who was referred to the cornea clinic with a case of keratitis. He was treated with topical antibiotics. After full resolution of keratitis, his condition was complicated by extensive corneal neovascularisation. A trial of photochemical corneal collagen CXL with riboflavin/ultraviolet A resulted in a dramatic improvement and resolution of the corneal neovascularisation. Thus, we can conclude that corneal collagen CXL could be a promising procedure to treat certain cases of extensive corneal neovascularisation.
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7

Cheng, Jacob YC, Doric WK Wong, and Chong Lye Ang. "Intraocular Avastin (Bevacizumab) for Neovascularisation of the Iris and Neovascular Glaucoma." Annals of the Academy of Medicine, Singapore 37, no. 1 (January 15, 2008): 72–74. http://dx.doi.org/10.47102/annals-acadmedsg.v37n1p72.

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Introduction: The aim of this study was to determine the effectiveness of intraocular injections of bevacizumab for neovascularisation of the iris and neovascular glaucoma. Clinical Picture: Three patients with neovascularisation of the iris due to various causes were recruited. Treatment: Patients were treated with intraocular bevacizumab. Outcome: Neovascularisation of the iris was noted to have completely regressed as early as 3 days after the injection and in all the patients (100%) within 8 days after injection. They were followed up for at least 1 month with no clinical evidence of recurrence. Visual acuity remained stable or improved, and the intraocular pressure was controlled in all the 3 patients’ eyes. Vitreous haemorrhage also cleared. No signs of inflammation or complications were observed. Conclusion: Intraocular injection of bevacizumab is effective and safe for patients with neovascularisation of the iris and neovascular glaucoma with or without vitreous haemorrhage. Key words: Intravitreal, Vascular endothelial growth factor, Vitreous haemorrhage
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8

Buragohain, Suklengmung, Harsha Bhattacharjee, and Henal Javeri. "Capsular neovascularisation in uveitis." Indian Journal of Ophthalmology - Case Reports 1, no. 3 (2021): 458. http://dx.doi.org/10.4103/ijo.ijo_3625_20.

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9

Faraj, L. A., D. G. Said, and H. S. Dua. "Evaluation of corneal neovascularisation." British Journal of Ophthalmology 95, no. 10 (September 21, 2011): 1343–44. http://dx.doi.org/10.1136/bjophthalmol-2011-300856.

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10

Stavrou, D. "Neovascularisation in wound healing." Journal of Wound Care 17, no. 7 (July 2008): 298–302. http://dx.doi.org/10.12968/jowc.2008.17.7.30521.

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11

Sunness, J. S. "Choroidal neovascularisation and atrophy." British Journal of Ophthalmology 90, no. 4 (April 1, 2006): 398–99. http://dx.doi.org/10.1136/bjo.2005.084830.

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12

Sivaprasad, S., and A. T. Moore. "Choroidal neovascularisation in children." British Journal of Ophthalmology 92, no. 4 (March 27, 2008): 451–54. http://dx.doi.org/10.1136/bjo.2007.124586.

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13

Binns, Malcolm, and Robert W. H. Pho. "Neovascularisation of the epiphysis." Microsurgery 12, no. 1 (1991): 9–13. http://dx.doi.org/10.1002/micr.1920120103.

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14

Carrozzo, Alessandro, Jobe Shatrov, Abdo El Helou, Francesco Pettinari, Ali Alayane, Ahmad Abed Ali, Julien Clechet, Thais Dutra Vieira, and Bertrand Sonnery-Cottet. "Ultrasound-guided electrocoagulation of neovascularisation for persistent patellar tendinopathy in athletes: a cohort study of 25 patients with a mean follow-up of 5 years from the SANTI Study Group." BMJ Open Sport & Exercise Medicine 10, no. 1 (March 2024): e001900. http://dx.doi.org/10.1136/bmjsem-2024-001900.

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BackgroundPatellar tendinopathy (PT) is a common condition characterised by persistent patellar tendon pain and dysfunction, particularly in athletes. Neovascularisation is frequently observed in the PT and is associated with increased pain. Ultrasound-guided electrocoagulation of neovascularisation has emerged as a minimally invasive alternative treatment for recalcitrant PT.Hypothesis/purposeThe purpose of this study was to evaluate the clinical outcomes of ultrasound-guided electrocoagulation of neovascularisation in athletes with persistent PT.Study designCase series; level of evidence, IV.MethodsA retrospective analysis of prospectively collected data was performed on 25 athletes who underwent ultrasound-guided electrocoagulation of neovascularisation for recalcitrant PT. Clinical outcomes including complications, reinterventions and patient-reported outcome measures were recorded. Comparisons between variables were assessed using χ2test or Fisher’s exact test for categorical variables and Student’s t-test or Wilcoxon test for quantitative variables.Results25 patients were included in the final analysis. 96% returned to their preoperative activity level at a mean of 3.8 months. At a mean follow-up of 5 years 4% did not receive significant benefit from electrocoagulation therapy. Significant improvements were observed in outcome measures, including the Victorian Institute of Sport Assessment Questionnaire for Patients with Patellar Tendinopathy, Kujala score, modified Blazina score and Visual Analogue Scale for pain.ConclusionUltrasound-guided electrocoagulation of neovascularisation for persistent PT in elite athletes resulted in a low complication rate, a high rate and rapid return to sport and a significant improvement in outcome measures.
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15

Bainbridge, James W., Vanya Loroch, Eric Viaud, and Claus Cursiefen. "Beyond Anti-VEGFs – Anti-Insulin Receptor Substrate-1 Oligonucleotides as a Novel Approach to Ocular Neovascular Disorders." European Ophthalmic Review 06, no. 03 (2012): 190. http://dx.doi.org/10.17925/eor.2012.06.03.190.

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Angiogenesis is a complex process that is vital to health but is also a driving factor behind a broad range of malignant, ischaemic, inflammatory, infectious and immune disorders. For optimal efficacy and safety, therapies aimed at preventing angiogenic-mediated disorders must differentiate between healthy and pathological angiogenesis or neovascularisation. Aganirsen is an antisense oligonucleotide that inhibits the insulin receptor substrate (IRS)-1 angiogenic pathway by targeting the IRS-1 messenger RNA. To date, studies of aganirsen have focused mainly on ocular disorders because of the ability to assess non-invasively the effect of the drug on neovascularisation and to address the unmet need for effective therapies in these blinding disorders. Aganirsen (GS-101) eye drops inhibit progressive corneal neovascularisation and appear to be well tolerated. The drug may offer an alternative and/or adjunct to intraocular anti-vascular endothelial cell growth factor (VEGF) agents, which are the current reference standards to prevent neovascularisation in retinal diseases. This is because it has a different and potentially complementary mechanism of action and can be administered topically. Antisense oligonucleotides targeting IRS-1 may present a valuable new approach to control pathological angiogenesis in the eye and elsewhere.
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16

Diamond, Michael Adam, Sze Wah Samuel Chan, Xun Zhou, Yelena Glinka, Eileen Girard, Yeni Yucel, and Neeru Gupta. "Lymphatic vessels identified in failed corneal transplants with neovascularisation." British Journal of Ophthalmology 103, no. 3 (October 22, 2018): 421–27. http://dx.doi.org/10.1136/bjophthalmol-2018-312630.

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BackgroundCorneal transplant failure with neovascularisation is a leading indication for full-thickness grafts in patients. Lymphangiogenesis is implicated in the pathology of graft failure, and here we systematically evaluate failed human corneal transplants with neovascularisation for the presence of lymphatic vessels.MethodsNine failed grafts with neovascularisation, based on H&E staining with subsequent immunoperoxidase staining for CD31, a blood vessel marker, were selected. Lymphatics were investigated by immunohistochemical and immunofluorescence approaches using podoplanin as a lymphatic marker. In two of nine cases, fluorescence in situ hybridisation (FISH) was used for detection of lymphatic mRNAs including podoplanin, VEGFR-3 and LYVE-1. All immunofluorescence and FISH samples were compared with positive and negative controls and visualised by confocal microscopy.ResultsCorneal neovascularisation was established in all cases by H&E and further confirmed by CD31 immunoreactive profiles. Immunohistochemistry for the podoplanin antibody was positive in all cases and showed morphologies ranging from distinct luminal structures to elongated profiles. Simultaneous immunofluorescence using CD31 and podoplanin showed lymphatic vessels distinct from blood vessels. Podoplanin immunofluorescence was noted in seven of nine cases and revealed clear lumina of varying sizes, in addition to lumen-like and elongated profiles. The presence of lymphatic mRNA was confirmed by FISH studies using a combination of at least two of podoplanin, VEGFR-3 and LYVE-1 mRNAs.ConclusionsThe consistent finding of lymphatic vessels in failed grafts with neovascularisation implicates them in the pathogenesis of corneal transplant failure, and points to the lymphatics as a potential new therapeutic target.
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17

Oki, Aqsa Sjuhada, Moch Febi Alviansyah, Christian Khoswanto, Retno Pudji Rahayu, and Muhammad Luthfi. "Acceleration of post-tooth extraction socket healing after continuous aerobic and anaerobic physical exercise in Wistar rats (Rattus norvegicus)." Dental Journal (Majalah Kedokteran Gigi) 53, no. 4 (November 24, 2020): 196. http://dx.doi.org/10.20473/j.djmkg.v53.i4.p196-200.

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Background: Physical exercise has been proven to accelerate wound healing. Physical training itself consists of aerobic (continuous training) and anaerobic (interval training) exercise. The effectiveness of continuous physical exercise on post-tooth extraction wound healing is the focus of this study. Purpose: This study aims to investigate the differences in post-tooth extraction wound healing in Wistar rats (Rattus norvegicus) after aerobic and anaerobic exercise based on the number of fibroblasts and neovascularisation. Methods: Wistar rats were divided into three groups: the control group (K1); K2 undertook continuous aerobic exercise, swimming at 50% maximum swimming capacity (MSC) with an additional 3% bodyweight load; K3 undertook anaerobic continuous exercise, swimming at 65% MSC with a 6% load. The rats swam three times per week for six weeks. The number of fibroblasts and neovascularisation were examined three days after tooth extraction. Data was analysed using the one-way analysis of variance (ANOVA) and Least Significant Difference (LSD) tests (p<0.05). Results: There was a significant difference in the number of fibroblasts between the K2 and K3 groups. There was no significant difference between K2 and K3 in the amount of neovascularisation. Conclusion: There were differences in the number of fibroblasts but not neovascularisation after tooth extraction in Wistar rats given aerobic and anaerobic continuous training.
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18

Holló, Gábor. "Diabetic neovascularisation and secondary glaucoma." Orvosi Hetilap 152, no. 29 (July 2011): 1167–70. http://dx.doi.org/10.1556/oh.2011.29042.

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Neovascular glaucoma develops from intraocular neovascularisation in diabetes mellitus. Neovascularisation is a consequence of hypoxia-induced production of vascular endothelial growth factor-A. Neovascular glaucoma is one of the most serious, sight-threatening late complications of diabetes. Several intraocular pressure lowering drugs, surgical and adjunctive laser treatments have been used to treat this disease, but the efficacy of the interventions is limited. The role of vascular endothelial growth factor-A blocking therapy in the treatment of neovascular glaucoma remains to be determined. Development of neovascularisation, however, can be prevented with adequate long-term glycemic and lipid control, effective treatment of arterial hypertension and optimal timing of adequate panretinal photocoagulation, in the majority of the cases. Unfortunately, in clinical practice diabetic neovascular glaucoma is more frequently experienced in Hungary than would be expected based on the variety of available therapeutic possibilities. In order to increase the success of prevention both cooperation of general practitioners, diabetologists, dietitians and ophthalmologists, and compliance of diabetic patients need to be improved. Orv. Hetil., 2011, 152, 1167–1170.
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19

Augustin, Albert J., and Indre Offermann. "Combination Therapy for Choroidal Neovascularisation." Drugs & Aging 24, no. 12 (2007): 979–90. http://dx.doi.org/10.2165/00002512-200724120-00002.

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20

Cheung, C. M. G., O. M. Durrani, and P. Stavrou. "Peripapillary choroidal neovascularisation in sarcoidosis." Ocular Immunology and Inflammation 10, no. 1 (January 2002): 69–73. http://dx.doi.org/10.1076/ocii.10.1.69.10324.

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21

Groeneveld, Erwin, and Paul Eliadis. "Interferon for subfoveal choroidal neovascularisation." Australian and New Zealand Journal of Ophthalmology 21, no. 2 (May 1993): 133–34. http://dx.doi.org/10.1111/j.1442-9071.1993.tb00769.x.

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22

Kaplan, H. "Submacular surgery for choroidal neovascularisation." British Journal of Ophthalmology 80, no. 2 (February 1, 1996): 101. http://dx.doi.org/10.1136/bjo.80.2.101.

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23

Lee, M. S. "Choroidal neovascularisation associated with meningioma." British Journal of Ophthalmology 89, no. 10 (October 1, 2005): 1384–85. http://dx.doi.org/10.1136/bjo.2005.071696.

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24

Postelmans, L., P. Coquelet, C. Verougstraete, and F. Willermain. "Treatment of peripapillary choroidal neovascularisation." British Journal of Ophthalmology 92, no. 5 (April 25, 2008): 721–22. http://dx.doi.org/10.1136/bjo.2007.135095.

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25

Yip, Vivien C., Leonard W. Yip, and Augustinus Laude. "Subconjunctival bevacizumab for iris neovascularisation." Lancet Diabetes & Endocrinology 2, no. 6 (June 2014): 449–50. http://dx.doi.org/10.1016/s2213-8587(14)70070-1.

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26

Cann, StephenA, JohannesP van Netten, TearaL Ashby, MichaelJ Ashwood-Smith, and NicholasG van der Westhuizen. "Role of lymphagenesis in neovascularisation." Lancet 346, no. 8979 (September 1995): 903. http://dx.doi.org/10.1016/s0140-6736(95)92744-1.

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27

Rowson, Neil J., John K. G. Dart, and Roger J. Buckley. "Corneal neovascularisation in acute hydrops." Eye 6, no. 4 (July 1992): 404–6. http://dx.doi.org/10.1038/eye.1992.83.

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28

Graham, E. M., M. R. Stanford, J. S. Shilling, and M. D. Sanders. "Neovascularisation associated with posterior uveitis." British Journal of Ophthalmology 71, no. 11 (November 1, 1987): 826–33. http://dx.doi.org/10.1136/bjo.71.11.826.

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29

Ohnishi, Yoshitaka, Tatsuro Ishibashi, and Takuji Sagawa. "Fluorescein gonioangiography in diabetic neovascularisation." Graefe's Archive for Clinical and Experimental Ophthalmology 232, no. 4 (April 1994): 199–204. http://dx.doi.org/10.1007/bf00184005.

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30

Hummel, T., P. Burger, N. Frings, M. Hartmann, M. Broermann, C. Schwahn-Schreiber, D. Stenger, M. Stücker, and A. Mumme. "High ligation of the saphenofemoral junction is necessary!" Phlebologie 38, no. 03 (2009): 99–102. http://dx.doi.org/10.1055/s-0037-1622261.

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SummaryNeovascularisation can compromise the success of high ligation and resection of the greater saphenous vein. Studies using duplexultrasound to classify recurrent groin veins have described rates of neovascularisation as high as 60% and raised the question whether high ligation is actually able to prevent groin recurrences. In the present study, recurrent groin veins were excised and examined histologically in order to prove whether neovascularisation is the main cause for sapheno-femoral recurrences. Patients, methods: 419 patients accounting for 458 legs with clinically symptomatic groin recurrences were included in a country-wide multicenter study. The recurrent groin veins were excised in a standardized fashion and subsequently divided into the different types of recurrence based on histopathological criteria. Results: 427 specimen (93%) were available for histopathological examination. In 69 cases (16.2%) a neovascularisation was found to be the cause of recurrence. 311 specimen (72.8%) contained a long residual stump of the greater saphenous vein, out of which 32 (7.5%) showed additional neovascularisation at the site of the ligation. In 29 cases (6.8%) a venous side branch was found to be the recurrent groin vein. 11 specimen (2.6%) did not contain any evidence of venous material and in another 7 cases (1.6%) it was not possible to clearly identify the cause of recurrence during the histo pathological workup. Conclusion: The high rates of neovascularisation described in several duplex ultrasound studies could not be confirmed in our investigation. Recurrences seem to be mainly caused by a technically incorrect initial operation which leaves a long residual stump of the saphenous vein in place. Following a technically correct high ligation, clinically relevant recurrences appear to be rare. This finding underlines the necessity of a high ligation of the saphenous vein according to current guidelines.
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31

De Maeseneer, M. G., I. F. Tielliu, P. E. Van Schil, S. G. De Hert, and E. J. Eyskens. "Clinical Relevance of Neovascularisation on Duplex Ultrasound in the Long-Term Follow-up after Varicose Vein Operation." Phlebology: The Journal of Venous Disease 14, no. 3 (September 1999): 118–22. http://dx.doi.org/10.1177/026835559901400306.

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Objective: To evaluate the clinical relevance of neovascularisation at the saphenous ligation site. Design: Long-term follow-up after previous varicose vein surgery in a single patient group. Setting: Vascular clinic of a university hospital. Patients: Eighty-two patients (106 limbs) with a mean follow-up period of 56 months after correct saphenous ligation were submitted to duplex scanning. Intervention: Clinical assessment and colour duplex scanning of all the operated limbs. Reintervention in 15 limbs with perioperative evaluation of recurrent veins. Main outcome measures: Limbs with and without recurrent varicose veins were classified according to the degree of neovascularisation: grade 0 = no new communicating veins, grade 1 = tiny new vein with diameter <4 mm, grade 2 = new communicating vein with diameter >4 mm and pathological reflux. On reintervention the presence of neovascular veins at the site of the previous ligation was checked. Results: In 68 limbs without recurrent varicose veins, grade 0 was observed in 50 limbs (74%), grade 1 in 12 limbs (18%) and grade 2 in six limbs (9%). In 38 limbs with recurrent varicose veins, grade 0 was diagnosed in eight limbs (21%), grade 1 in four limbs (11%) and grade 2 in 26 limbs (68%). In 15 limbs with recurrent varicose veins and grade 2 neovascularisation, reintervention confirmed the duplex findings. Conclusions: The presence of grade 2 neovascularisation was associated with the recurrence of varicose veins, suggesting a causal relationship.
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32

Haj Najeeb, Bilal, Gabor G. Deak, Ursula Margarethe Schmidt-Erfurth, and Bianca S. Gerendas. "RAP study, report 1: novel subtype of macular neovascularisation type III, cilioretinal MNV3." British Journal of Ophthalmology 105, no. 1 (March 11, 2020): 113–17. http://dx.doi.org/10.1136/bjophthalmol-2019-315311.

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PurposeTo report on patients with macular neovascularisation type III (MNV3) arising from cilioretinal arteries (CRAs) (cilioretinal macular neovascularisation type III (cMNV3)).MethodsWe reviewed baseline examinations of patients with neovascular age-related macular degeneration using multimodal imaging. We determined the type and distribution of MNV lesions in each cMNV3 case, the range of distances from the fovea, existence of exudative maculopathy, intraretinal haemorrhage and other morphological characteristics. 50 consecutive eyes with usual MNV3 without CRA were included as a control group.Results102 eyes of 102 patients were identified with MNV3 lesions. Among these, we found 12 eyes (12%) with cMNV3, 84 eyes (82%) with usual MNV3 without CRA and 6 eyes (6%) with usual MNV3 with CRA. Ten cases of cMNV3 had one lesion, and two cases had two lesions. The lesions were distributed equally between the superior and inferior halves of the macula, whereas in the nasal and temporal halves, there were 8 (57%) and 6 (43%) lesions, respectively. All cMNV3 lesions were located between 500 and 1500 µm from the central fovea except one, which was located between 1500 and 3000 µm. None of the lesions had macular neovascularisation type I (MNV1) or macular neovascularisation type II (MNV2) elsewhere in both groups. Exudative maculopathy and intraretinal haemorrhage were found in seven (88%) and five (63%) of the eight pure cMNV3 cases, respectively.ConclusioncMNV3 can be solitary or multiple, isolated or accompanied with usual MNV3 lesions, but not with concurrent MNV1 or MNV2. It is frequently associated with extensive exudative maculopathy, intraretinal haemorrhage and subretinal fluid.
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33

&NA;. "Changing times for intraocular neovascularisation, oedema." Inpharma Weekly &NA;, no. 1654 (September 2008): 9. http://dx.doi.org/10.2165/00128413-200816540-00015.

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34

Tuncel, Alper, Merdan Serin, and Mehmet Bayramicli. "Venous component in scar penetrating neovascularisation." Journal of Plastic Surgery and Hand Surgery 52, no. 1 (May 9, 2017): 47–52. http://dx.doi.org/10.1080/2000656x.2017.1319848.

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35

Lee, D. K. "Serpiginous choroidopathy presenting as choroidal neovascularisation." British Journal of Ophthalmology 87, no. 9 (September 1, 2003): 1184–85. http://dx.doi.org/10.1136/bjo.87.9.1184.

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Berger, Lisa, and Bernhard M. Stoffelns. "Photodynamic Therapy in Subfoveal Choroidal Neovascularisation." Medical Laser Application 17, no. 4 (January 2002): 331–40. http://dx.doi.org/10.1078/1615-1615-00078.

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AI-Husainy, S., P. Stavrou, and M. W. Hope-Ross. "Alkali injury complicated by choroidal neovascularisation." Eye 14, no. 6 (November 2000): 904–5. http://dx.doi.org/10.1038/eye.2000.247.

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Mehta, J. S., A. S. Jacks, V. Maurino, and A. M. P. Hamilton. "Neovascularisation in a patent chorioretinal anastomosis." Eye 14, no. 6 (November 2000): 916–18. http://dx.doi.org/10.1038/eye.2000.256.

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Menzel-Severing, J. "Emerging techniques to treat corneal neovascularisation." Eye 26, no. 1 (October 7, 2011): 2–12. http://dx.doi.org/10.1038/eye.2011.246.

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McLEOD, D. "Entry site neovascularisation after diabetic vitrectomy." British Journal of Ophthalmology 84, no. 8 (August 1, 2000): 810–12. http://dx.doi.org/10.1136/bjo.84.8.810.

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Lee, J. "Preretinal neovascularisation associated with choroidal melanoma." British Journal of Ophthalmology 85, no. 11 (November 1, 2001): 1309–12. http://dx.doi.org/10.1136/bjo.85.11.1309.

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Aisenbrey, S., F. Gelisken, P. Szurman, and K. U. Bartz-Schmidt. "Surgical treatment of peripapillary choroidal neovascularisation." British Journal of Ophthalmology 91, no. 8 (February 14, 2007): 1027–30. http://dx.doi.org/10.1136/bjo.2006.108118.

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Binder, S. "Surgical treatment of peripapillary choroidal neovascularisation." British Journal of Ophthalmology 91, no. 8 (July 17, 2007): 990–91. http://dx.doi.org/10.1136/bjo.2007.114009.

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Bradbury, Jane. "Integrin antagonists may prevent retinal neovascularisation." Lancet 347, no. 9010 (May 1996): 1249. http://dx.doi.org/10.1016/s0140-6736(96)90751-5.

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Gupta, B., S. Parvizi, and M. D. Mohamed. "Bietti crystalline dystrophy and choroidal neovascularisation." International Ophthalmology 31, no. 1 (October 23, 2010): 59–61. http://dx.doi.org/10.1007/s10792-010-9406-8.

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Coscas, Gabriel. "Subretinal neovascularisation in senile macular degeneration." Eye 1, no. 3 (May 1987): 364–78. http://dx.doi.org/10.1038/eye.1987.56.

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Boulton, Mike, Bharti Patel, Asud Khaliq, Patrick Moriarty, John Jarvis-Evans, and David McLeod. "Modulators and milieu in preretinal neovascularisation." Eye 6, no. 6 (November 1992): 560–65. http://dx.doi.org/10.1038/eye.1992.122.

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Inglesby, D. V., G. S. Turner, W. E. Schulenburg, and E. M. Kohner. "Photocoagulation for peripheral neovascularisation in diabetes." British Journal of Ophthalmology 69, no. 3 (March 1, 1985): 157–61. http://dx.doi.org/10.1136/bjo.69.3.157.

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Campochiaro, Peter A. "Ocular neovascularisation and excessive vascular permeability." Expert Opinion on Biological Therapy 4, no. 9 (September 2004): 1395–402. http://dx.doi.org/10.1517/14712598.4.9.1395.

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SILVA, R., TY WONG, and F. ASMUS. "Prognostic factors in myopic choroidal neovascularisation." Acta Ophthalmologica 92 (August 20, 2014): 0. http://dx.doi.org/10.1111/j.1755-3768.2014.3471.x.

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