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Reconstruction
Published in Karl H. Pang, Nadir I. Osman, James W.F. Catto, Christopher R. Chapple, Basic Urological Sciences, 2021
Nadir I. Osman, Karl H. Pang, Christopher R. Chapple
Grafts blood supply develops by a process called ‘take’:Imbibition: graft absorbs (imbibe = drinks) nutrients from the underlying recipient bed (0−48 hours). Nutrients + waste are passed between the graft + recipient bed through passive diffusion. Graft temperature is lower than body temperature.Inosculation: blood vessels in the graft grow to meet the vessels (inosculate = kiss) of the recipient bed (48−96 hours). Graft temperature = body temperature.Neovascularisation: new blood vessels form between the graft and recipient tissues.
Swarm Intelligence and Evolutionary Algorithms for Diabetic Retinopathy Detection
Published in Sandeep Kumar, Anand Nayyar, Anand Paul, Swarm Intelligence and Evolutionary Algorithms in Healthcare and Drug Development, 2019
Sachin Bhandari, Radhakrishna Rambola, Rajani Kumari
The classification of PDR contains neovascularisation, rubeosis, neovascularization at a disc as signs: Neovascularization (NV): It is stated as a typical emergence of new blood vessels that usually emerges on the internal surfaces of retina [1]. This is caused by angiogenic growth factor increased by hypoxic retinal tissues in an attempt to revascularization of the hypoxic retina, so there is lack of oxygen in these vascular endothelial growth factors and they create new blood vessels and neovascularization. The problem with the new blood vessels is that they are irregular, they are not formed well, they are fragile and then they burst and leak. The sign of neovascularisation is mottled mess of very fine blood vessels.Rubeosis: It occurs with PDR and rubeosis appears as neovascularization but it is neovascularization at iris and this is definitely not a normal state of affairs.Neovascularization disc (NVD): The term NVD in a patient file that stands for neovascularization elsewhere and that means neovascularization occurring somewhere in the retina not at the disc.
Pegaptanib sodium therapy
Published in A Peyman MD Gholam, A Meffert MD Stephen, D Conway MD FACS Mandi, Chiasson Trisha, Vitreoretinal Surgical Techniques, 2019
Lawrence J Singerman, Mithlesh C Sharma, Joan H Hornik
Ideally, treatment for neovascularization would selectively inhibit pathologic neovascularization while avoiding adverse effects that might result from nonselective inhibition of physiologic vascularization. In preclinical animal models, researchers compared the effects of pegaptanib sodium with those of a pan-VEGF blocker that blocks VEGF isoforms. The research showed that the growth of pathologic vascularization was inhibited by pegaptanib sodium as well as by the pan-VEGF blocker. However, the pan-VEGF blocker also suppressed normal growth of physiologic vascularization, whereas pegaptanib sodium had little to no effect on it.4
Follow-up outcomes of different bypass surgical modalities for adults with ischaemic-type moyamoya disease
Published in British Journal of Neurosurgery, 2023
Peng Gao, Di Chen, Shanpeng Yuan, Tengxiao Kong, Dongtao Zhang, Xuqiang Zhu, Xueyuan Li, Yingwei Zhen, Dongming Yan
Six months after the operation, the patients came to our hospital for DSA and cerebral perfusion imaging and were then followed up face-to-face or by phone every 6 months. If the patients had uncomfortable symptoms, they were recorded in detail, and the doctors of our hospital were informed as soon as possible. Recurrent stroke events and mRS scores were recorded at each follow-up. If the mRS score of the last follow-up was less than the preoperative mRS score, the neurological function was said to have improved and was rated as good when the mRS score was less than 2. Neovascularization was assessed according to the method recommended by Matsushima et al. as follows: Grade A, the range of neovascularization is more than 2/3 of the blood supply area of the middle cerebral artery; grade B, 1/3 to 2/3; grade C, less than 1/3.21 The physician did not know the baseline characteristics of the patient during the follow-up period.
Correlation Between Proteolytic Enzymes and Microangiogenesis in Degenerative Intervertebral Disc Nucleus
Published in Journal of Investigative Surgery, 2021
Consistent with earlier reports, neovascularization is enhanced [15]. Infiltration of the epidural vena cava, vertebral body margin or PLL has been considered to be the origin of new blood vessels for disc herniation [18]. The pathogenesis of neovascularization differs in the location of the tissue. Small blood vessels may be necessary to strengthen the damaged disc and to indicate the repair process. The granulation tissue with blood vessels is mainly formed at the edge of the intervertebral disc tissue, and the accumulation of strong inflammatory factors directly promotes the absorption of tissue [19]. Studies have found that the severity of tissue degeneration is significantly associated with the level of neovascularization in disc herniation tissue. Some authors have demonstrated that degenerative changes in intervertebral disc tissue are associated with neovascularization. Karamouzian et al. [20] found that the incidence of angiogenesis was significantly associated with microcalcification in nucleus pulposus specimens. Different protein, collagen and proteoglycan breakdown products may induce angiogenesis at the molecular level [21]. For example, growth factors are considered to be important regulators of neovascularization and intervertebral disc degeneration. VEGF may play a role in neovascularization of diseased or damaged intervertebral disc tissue [22].
Vascular Regeneration for Ischemic Retinopathies: Hope from Cell Therapies
Published in Current Eye Research, 2020
Pietro Maria Bertelli, Edoardo Pedrini, Jasenka Guduric-Fuchs, Elisa Peixoto, Varun Pathak, Alan W. Stitt, Reinhold J. Medina
The presence of vascular complications allows a further categorization of RVOs into edematous, ischemic, and miscellaneous.27 The development of a thrombus in the retinal vasculature is associated with decreased blood flow, damage of the endothelium leading to vascular leakage and edema.26 Additionally, the poor retinal perfusion in RVO is also associated with neuronal cell death and photoreceptor apoptosis. In accordance with that, thinning of the macula, retinal nerve fiber, ganglion cell and inner plexiform layers was reported in RVO.28 Long-term ischemic environment leads to secretion of inflammatory and angiogenic factors, such as VEGF. These molecules cause worsening of the pathology in RVO and play a central role in the initialization of retinal neovascularization.24 Neovascularization is directly correlated to the level of occlusion and can be the starting point of further complications, such as neovascular glaucoma, hemorrhage in the vitreous and also retinal detachment.24,26