The blood-retinal barrier, or the BRB, is part of the blood-ocular barrier that consists of cells that are joined tightly together to prevent certain substances from entering the tissue of the retina. It consists of non-fenestrated capillaries of the retinal circulation and tight-junctions between retinal epithelial cells preventing passage of large molecules from choriocapillaris into the retina. The blood retinal barrier has two components: the retinal vascular endothelium and the retinal pigment epithelium. Retinal blood vessels that are similar to cerebral blood vessels maintain the inner blood-ocular barrier. This physiological barrier comprises a single layer of non-fenestrated endothelial cells, which have tight junctions. These junctions are impervious to tracer, so many substances can affect the metabolism of the eyeball. The retinal pigment epithelium maintains the outer blood-retinal barrier. Diabetic retinopathy, eye damage that frequently occurs as a result of diabetes, is related ...
Purpose : In patients with ocular toxoplasmosis, disruption of retinal pigment epithelium is frequently observed. The retinal pigment epithelial layer constitutes outer blood retinal barrier (BRB) that lies between retina and leaky choroidal vasculature. In this study, we investigated the effect of monocytes infected with Toxoplasma gondii on in vitro model of outer BRB. Methods : Retinal pigment epithelial cells, ARPE-19, were cultivated on transwell to form a confluent monolayer. Then, human monocytic cells, THP-1, infected with Toxoplasma gondii or their conditioned medium were treated and the barrier function was evaluated by measurement of transepithelial electrical resistance (TEER) and immunocytochemistry of tight junction proteins. Additional treatment with FAK inhibitor (PF-573228) or neutralizing antibody against IL-8 was performed to investigate the associated signaling pathway. Results : Twenty-four hours after the treatment with infected monocytes or their conditioned medium, TEER ...
Breakdown of the blood-brain barrier (BBB) or inner blood-retinal barrier (BRB), induced by pathologically elevated levels of vascular endothelial growth factor (VEGF) or other mediators, can lead to vasogenic edema and significant clinical problems such as neuronal morbidity and mortality, or vision loss. Restoration of the barrier function with corticosteroids in the brain, or by blocking VEGF in the eye are currently the predominant treatment options for brain edema and diabetic macular edema, respectively. However, corticosteroids have side effects, and VEGF has important neuroprotective, vascular protective and wound healing functions, implying that long-term anti-VEGF therapy may also induce adverse effects. We postulate that targeting downstream effector proteins of VEGF and other mediators that are directly involved in the regulation of BBB and BRB integrity provide more attractive and safer treatment options for vasogenic cerebral edema and diabetic macular edema. The endothelial cell-specific
The purpose of this study was to characterize the cell surface proteome of native compared to cultured equine retinal pigment epithelium (RPE) cells. The RPE plays an essential role in visual function and represents the outer blood-retinal barrier. We are investigating immunopathomechanisms of equine recurrent uveitis, an autoimmune inflammatory disease in horses leading to breakdown of the outer blood-retinal barrier and influx of autoreactive T-cells into affected horses vitrei. Cell surface proteins of native and cultured RPE cells from eye-healthy horses were captured by biotinylation, analyzed by high resolution mass spectrometry coupled to liquid chromatography (LC MS/MS), and the most interesting candidates were validated by PCR, immunoblotting and immunocytochemistry. A total of 112 proteins were identified, of which 84% were cell surface membrane proteins. Twenty-three of these proteins were concurrently expressed by both cell states, 28 proteins exclusively by native RPE cells. Among the
The blood-retinal barrier (BRB) plays an important role in the homeostatic regulation of the microenvironment in the retina. It consists of inner and outer components, the inner BRB (iBRB) being formed by the tight junctions between neighbouring retinal capillary endothelial cells and the outer barrier (oBRB) by tight junctions between retinal pigment epithelial cells. Astrocytes, Müller cells and pericytes contribute to the proper functioning of the iBRB. In many clinically important conditions including diabetic retinopathy, ischaemic central retinal vein occlusion, and some respiratory diseases, retinal hypoxia results in a breakdown of the iBRB. Disruption of the iBRB associated with increased vascular permeability, results in vasogenic oedema and tissue damage, with consequent adverse effects upon vision. Factors such as enhanced production of vascular endothelial growth factor (VEGF), NO, oxidative stress and inflammation underlie the increased permeability of the iBRB and inhibition of ...
Purpose: VEGF-related signal transduction and gene regulatory networks play central roles in the vascular pathology of several retinal diseases: ROP, diabetic retinopathy, AMD, Norries disease and FEVR. While mechanisms are often explored in cell culture, there is need for in vivo models that are amenable to functional and molecular analysis during blood-retinal barrier (BRB) disruption and inflammatory response. We developed an intravitreal VEGF-injection model that provides a new platform for functional assessment of BRB disruption and countermeasures using ERG, Fluorescein angiography (FA) and Optical Coherence Tomography (OCT) in a single session of anesthesia.. Methods: Retinas of Long Evans rats were documented with bright-field imaging, FA, & OCT. Some animals received ERG, FA and OCT during a single session in an advanced ocular imaging suite of the Pediatric Retinal Research Laboratory. Subsequently, rats received a single intravitreal injection of recombinant human VEGF (35-gage ...
Rather than being a non-specific reaction to a noxious stimulus, breakdown of the capillary blood-retinal barrier causing macular edema appears to be dependent on a number of active processes which may be open to pharmacological manipulation. Extracellular influences which may affect barrier function include serum and neighboring cell types, which act though cytokines, such as vascular endothelial growth factor and transforming growth factor-ß, and other factors. A number of intracellular pathways acting on the cytoskeleton and components of the intercellular junctional complexes have been identified which mediate agonist-induced leak of the vascular endothelium. The further elucidation of these processes may be useful in the development of better treatments for breakdown of the inner blood-retinal barrier. ...
Researchers in Barcelona have developed a microfluidic chip that mimics the human blood-retinal barrier. The device contains several parallel compartments,
The device contains living cells and mimics the structure and physiological conditions of the blood-retinal barrier; it also enables testing...
Acute intensive insulin therapy is an independent risk factor for diabetic retinopathy. Here we demonstrate that acute intensive insulin therapy markedly increases VEGF mRNA and protein levels in the retinae of diabetic rats. Retinal nuclear extracts from insulin-treated rats contain higher hypoxia-inducible factor-1α (HIF-1α) levels and demonstrate increased HIF-1α-dependent binding to hypoxia-responsive elements in the VEGF promoter. Blood-retinal barrier breakdown is markedly increased with acute intensive insulin therapy but can be reversed by treating animals with a fusion protein containing a soluble form of the VEGF receptor Flt; a control fusion protein has no such protective effect. The insulin-induced retinal HIF-1α and VEGF increases and the related blood-retinal barrier breakdown are suppressed by inhibitors of p38 mitogen-activated protein kinase (MAPK) and phosphatidylinositol (PI) 3-kinase, but not inhibitors of p42/p44 MAPK or protein kinase C. Taken together, these findings ...
Acute intensive insulin therapy is an independent risk factor for diabetic retinopathy. Here we demonstrate that acute intensive insulin therapy markedly increases VEGF mRNA and protein levels in the retinae of diabetic rats. Retinal nuclear extracts from insulin-treated rats contain higher hypoxia-inducible factor-1α (HIF-1α) levels and demonstrate increased HIF-1α-dependent binding to hypoxia-responsive elements in the VEGF promoter. Blood-retinal barrier breakdown is markedly increased with acute intensive insulin therapy but can be reversed by treating animals with a fusion protein containing a soluble form of the VEGF receptor Flt; a control fusion protein has no such protective effect. The insulin-induced retinal HIF-1α and VEGF increases and the related blood-retinal barrier breakdown are suppressed by inhibitors of p38 mitogen-activated protein kinase (MAPK) and phosphatidylinositol (PI) 3-kinase, but not inhibitors of p42/p44 MAPK or protein kinase C. Taken together, these findings ...
Acute intensive insulin therapy is an independent risk factor for diabetic retinopathy. Here we demonstrate that acute intensive insulin therapy markedly increases VEGF mRNA and protein levels in the retinae of diabetic rats. Retinal nuclear extracts from insulin-treated rats contain higher hypoxia-inducible factor-1α (HIF-1α) levels and demonstrate increased HIF-1α-dependent binding to hypoxia-responsive elements in the VEGF promoter. Blood-retinal barrier breakdown is markedly increased with acute intensive insulin therapy but can be reversed by treating animals with a fusion protein containing a soluble form of the VEGF receptor Flt; a control fusion protein has no such protective effect. The insulin-induced retinal HIF-1α and VEGF increases and the related blood-retinal barrier breakdown are suppressed by inhibitors of p38 mitogen-activated protein kinase (MAPK) and phosphatidylinositol (PI) 3-kinase, but not inhibitors of p42/p44 MAPK or protein kinase C. Taken together, these findings ...
There are several mechanisms by which statins might exhibit anti-inflammatory effects in the eye [28]. Statins are known to inhibit the activation of Rho guanosine triphosphatase (GTPase), a key molecule in the endothelial ICAM-1-mediated pathway that facilitates lymphocyte migration [29-31]. Statins thus inhibit interactions between leukocytes and endothelial cells, preventing leukocyte transmigration from the vasculature, across the blood-retinal barrier [29, 32-34]. Endothelial cell nitric oxide synthase expression is up-regulated in the presence of statins, leading to higher levels of nitric oxide, which has protective effects on endothelial cells [35]. Statins also inhibit the formation of oxygen free radicals by endothelial cells [36, 37]. Thus, statins may act to stabilize the blood-ocular and blood-retinal barrier, transgression across which enables inflammatory mediators and immune activator cells to enter the anterior chamber, vitreous cavity, and retinal tissues. In addition, statins ...
The use of In vitro testing with living cells as an alternative to animal research has limitations like the difficulty to reproduce the interaction of cells. To
Placental Growth Factor Contributes to Micro-Vascular Abnormalization and Blood-Retinal Barrier Breakdown in Diabetic Retinopathy. Kowalczuk, Laura; Touchard, Elodie; Omri, Samy; Jonet, Laurent; Klein, Christophe; Valamanes, Fatemeh; Berdugo, Marianne; Bigey, Pascal; Massin, Pascale; Jeanny, Jean-Claude; Behar-Cohen, Francine // PLoS ONE;2011, Vol. 6 Issue 3, p1 Objective: There are controversies regarding the pro-angiogenic activity of placental growth factor (PGF) in diabetic retinopathy (DR). For a better understanding of its role on the retina, we have evaluated the effect of a sustained PGF overexpression in rat ocular media, using ciliary muscle... ...
Discussion. The present study demonstrated the functional involvement of SR-BI in the uptake of HDL-associated α-tocopherol by retinal capillary endothelial cells using an in vitro inner BRB model, TR-iBRB2 cells. Although the uptake process of fat-soluble micronutrients like vitamin E was assumed to be passive diffusion across the plasma membrane, recent reports have proposed SR-BI-mediated transport of α-tocopherol in the brain capillary endothelial cells and enterocytes [18,19,21]. In this study, [14C]α-tocopherol-HDL uptake by TR-iBRB2 cells exhibited a time-dependent increase and did not reach "steady-state" at least for 90 min, suggesting that, for the most part [14C]α-tocopherol-HDL uptake by TR-iBRB2 cells depends on influx mechanism(s). [14C]α-tocopherol-HDL uptake by TR-iBRB2 cells was reduced by 88% for 90 min at 4 °C compared with that at 37 °C (Figure 1A). This suggests the involvement of an energy-dependent carrier-mediated process, rather than passive diffusion. In turn, ...
The blood-retina barrier and blood-brain barrier (BRB/BBB) are selective and semipermeable and are critical for supporting and protecting central nervous system (CNS)-resident cells. Endothelial cells (ECs) within the BRB/BBB are tightly coupled, express high levels of Claudin-5 (CLDN5), a junctional protein that stabilizes ECs, and are important for proper neuronal function. To identify novel CLDN5 regulators (and ultimately EC stabilizers), we generated a CLDN5-P2A-GFP stable cell line from human pluripotent stem cells (hPSCs), directed their differentiation to ECs (CLDN5-GFP hPSC-ECs), and performed flow cytometry-based chemogenomic library screening to measure GFP expression as a surrogate reporter of barrier integrity. Using this approach, we identified 62 unique compounds that activated CLDN5-GFP. Among them were TGF-β pathway inhibitors, including RepSox. When applied to hPSC-ECs, primary brain ECs, and retinal ECs, RepSox strongly elevated barrier resistance (transendothelial electrical ...
Advanced glycation end products have been associated with numerous complications of diabetes (Ahmed, 2005). The levels of AGEs in the blood and vitreous humor of diabetic patients have been correlated with the clinical progression of diabetic retinopathy (Yokoi et al., 2005). Although the RPE expresses several pattern-recognizing receptors activated by AGEs, a direct causal relationship between AGEs and RPE dysfunction has not been addressed before. Using human glycated-albumin, we determined the effect of AGEs on the barrier function of the RPE. The RPE constitutes the outer blood-retina barrier and is responsible for fluid transport from the neural retina to the choroid. This transport counters the Starling forces across the RPE that drive fluid toward the retina (Maepea, 1992). As a result, increasing RPE permeability can contribute to the development of macular edema, a key component of diabetic retinopathy.. Our experiments demonstrated that the administration of human Glyc-alb reduced TEER ...
• The permeability of the blood-retina barrier was tested in rats with early streptozocin-induced diabetes. Two different tracer substances were used: fluoresce
Chronic hyperglycemia may cause growth factor alterations that are likely to participate in tissue remodeling typical for diabetic late complications. However, few details of such events are known. The ocular vitreous fluid allows studies of growth factor levels in human eyes (after vitrectomy). The vitreous is highly inert and protected by the blood-retina barrier and thus probably reflects growth factor production by the normal retina. Vitreous from patients with proliferative diabetic retinopathy (PDR) was compared with vitreous obtained from patients with nonproliferative eye disease and with vitreous from patients without diabetes but with marked neovascular proliferations due to ischemia. This design permits us to distinguish diabetes-related from non-diabetes-related alterations. Insulin-like growth factor I (IGF-I), IGF-II, IGF binding protein 2 (IGFBP-2), and IGFBP-3 were elevated 3-to 13-fold in nondiabetic retinal ischemia and 1.5- to 3-fold in PDR, indicating that the changes were ...
Nevroglia 0 domande The non-neuronal cells of the nervous system. They not only provide physical support, but also respond to injury, regulate the ionic and chemical composition of the extracellular milieu, participate in the BLOOD-BRAIN BARRIER and BLOOD-RETINAL BARRIER, form the myelin insulation of nervous pathways, guide neuronal migration during development, and exchange metabolites with neurons. Neuroglia have high-affinity transmitter uptake systems, voltage-dependent and transmitter-gated ion channels, and can release transmitters, but their role in signaling (as in many other functions) is unclear. ...
Névroglie 0 questions The non-neuronal cells of the nervous system. They not only provide physical support, but also respond to injury, regulate the ionic and chemical composition of the extracellular milieu, participate in the BLOOD-BRAIN BARRIER and BLOOD-RETINAL BARRIER, form the myelin insulation of nervous pathways, guide neuronal migration during development, and exchange metabolites with neurons. Neuroglia have high-affinity transmitter uptake systems, voltage-dependent and transmitter-gated ion channels, and can release transmitters, but their role in signaling (as in many other functions) is unclear. ...
|p|Many antioxidants, even some of the more potent ones, are unable to cross both your blood-brain and blood-retinal barriers to reach your brain, nervous system, and eyes.|/p| |p|Astaxanthin is different. It has the rare ability to cross these protectiv
The monolayer of endothelial cells lining the vessel wall forms a semipermeable barrier (in all tissue except the relatively impermeable blood-brain and inner retinal barriers) that regulates tissue-fluid homeostasis, transport of nutrients, and migration of blood cells across the barrier. Permeabil …
In choosing a model for evaluating the data for the present study, we faced a dilemma between an unbiased representation of the data and a parsimonious description of the essential physiological phenomena. The model used in the present study is based on simplifying assumptions. For example, the transit time of the nonexchanging ("large") vessels, t0, is assumed to be uniform and identical for sodium and rubidium. The membrane permeability for rubidium and the diameter of sinusoids are also assumed uniform. These simplifications may be responsible for small but systematic deviations of the model from the experimental data. Moreover, temporal fluctuations of liver blood flow due to the breathing movements of the animals may have led to minor distortions of the outflow profiles. Since for a majority of the animals, systematic deviations were not significant, the values obtained for the permeability surface area product may be regarded as valid approximations for the liver averages in all ...
The retinal pigment epithelium (RPE), the outer blood-retinal barrier in the eye, secretes many growth factors to support the normal functions of both the retina and the choroid. Dysfunction of RPE is believed to play a critical role in the pathogenesis of age-related macular degeneration (AMD). Advanced AMD can manifest in either geographic atrophy (dry AMD) or a neovascular form of the disease (wet AMD). Recently our studies indicated that bone morphogenetic protein-4 (BMP4), one growth factor of the transforming growth factor-β (TGF-β) superfamily, may be involved in the molecular switch that determines which advanced form of AMD an individual develops. We demonstrated that BMP4 was highly expressed in the macular RPE and adjacent extracellular matrix of dry AMD patients, and BMP4 mediated oxidative stress induced RPE cell senescence in vitro. However, BMP4 was immunohistochemically absent in RPE in subretinal choroidal neovascularization (CNV) membranes of wet AMD patients. This work ...
Objective and design A mathematical analysis of leukocytes accumulating in experimental autoimmune uveitis (EAU), using ordinary differential equations (ODEs) and incorporating a barrier to cell traffic. Materials and subjects Data from an analysis of the kinetics of cell accumulation within the eye during EAU. Methods We applied a well-established mathematical approach that uses ODEs to describe the behaviour of cells on both sides of the blood-retinal barrier and compared data from the mathematical model with experimental data from animals with EAU. Results The presence of the barrier is critical to the ability of the model to qualitatively reproduce the experimental data. However, barrier breakdown is not sufficient to produce a surge of cells into the eye, which depends also on asymmetry in the rates at which cells can penetrate the barrier. Antigen-presenting cell (APC) generation also plays a critical role and we can derive from the model the ratio for APC production under inflammatory ...
FT011M reduced retinal leukostasis and ICAM-1 mRNA levels in Ren-2 rats diabetic for 8 weeks.Non-diab, non-diabetic. Diab, diabetic. V, vehicle. (A to C) Microg
OBJECTIVE: To assess the effects of bevacizumab and everolimus, individually and combined, on CT perfusion (CTp) parameters in liver metastases from neuroendocrine tumors (mNET) and normal liver. METHODS: This retrospective study comprised 27 evaluable patients with mNETs who had participated in a two-arm randomized clinical trial of mono-therapy with bevacizumab (Arm B) or everolimus (Arm E) for 3 weeks, followed by combination of both targeted agents. CTp was undertaken at baseline, 3 and 9 weeks, to evaluate blood flow (BF), blood volume (BV), mean transit time (MTT), permeability surface area product (PS), and hepatic arterial fraction (HAF) of mNET and normal liver, using a dual-input distributed parameter physiological model ...
The RPE stores vitamin A, a precursor of the photopigments, and thus participates in their regeneration. There are four photopigments which are all bleached on exposure to light: rhodopsin (found in the rods, for night vision) and one for each of the three different types of cones (one for each of the primary colours). It synthesises glycosaminoglycans for the interphotoreceptor matrix, i.e. the material lying between and separating the photoreceptors.. Besides oxygen, the RPE selectively transports nutrients from the choroid to supply the outer third of the retina and removes the waste products of photoreceptor metabolism to be cleared by the choroidal circulation. By selective pumping of metabolites and the presence of its tight intercellular junctions, the RPE acts as a barrier, called the blood-retinal barrier, preventing access of larger or harmful chemicals to retinal tissue, thereby contributing to the maintenance of a stable and optimal retinal environment.8,9,10. The RPE has complex ...
The RPE stores vitamin A, a precursor of the photopigments, and thus participates in their regeneration. There are four photopigments which are all bleached on exposure to light: rhodopsin (found in the rods, for night vision) and one for each of the three different types of cones (one for each of the primary colours). It synthesises glycosaminoglycans for the interphotoreceptor matrix, i.e. the material lying between and separating the photoreceptors.. Besides oxygen, the RPE selectively transports nutrients from the choroid to supply the outer third of the retina and removes the waste products of photoreceptor metabolism to be cleared by the choroidal circulation. By selective pumping of metabolites and the presence of its tight intercellular junctions, the RPE acts as a barrier, called the blood-retinal barrier, preventing access of larger or harmful chemicals to retinal tissue, thereby contributing to the maintenance of a stable and optimal retinal environment.8,9,10. The RPE has complex ...
We report the second family recognised to have autosomal dominant vitreoretinochoroidopathy. The clinical features were (1) autosomal dominant inheritance; (2) peripheral, coarse pigmentary degeneration of the fundus for 360 degrees, with a relatively discrete posterior border in the equatorial region (this finding may be pathognomonic); (3) superficial punctate yellowish-white opacities in the retina; (4) various vascular abnormalities; (5) breakdown of the blood-retinal barrier; (6) retinal neovascularisation; (7) vitreous abnormalities; and (8) choroidal atrophy. Visual reduction was mainly due to macular oedema or vitreous haemorrhage. ...
One of the really special attributes of astaxanthin is its ability to cross the blood-brain and blood-retinal barrier to protect both the brain and eyes. This effect is quite unusual for carotenes. For example, popular carotenes like beta-carotene and lycopene do not cross either barrier. This effect of astaxanthin indicates that it may be particularly helpful in improving brain and eye health as well as protecting the brain against Alzheimers disease, macular degeneration, and other degenerative brain and eye disorders. Of course, it has other benefits as well, but my feelings are that this ability to cross into the brain and retina is what makes it really special.. Another interesting effect of astaxanthin is on red blood cells. Because red blood cells (RBCs) are more susceptible to being damaged by oxidative attack as we age, this can lead to impaired delivery of oxygen to our tissues. Astaxanthins effects on cell membranes may be especially important in RBCs. In a 2011 double-blind ...
Purpose: The outer limiting membrane (OLM) is considered to play a role in maintaining the structure of the retina through mechanical strength. However, the observation of junction proteins located at the OLM and its barrier permeability properties may suggest that the OLM may be part of the retinal barrier. Material and methods: Normal and diabetic rat, monkey, and human retinas were used to analyze junction proteins at the OLM. Proteome analyses were performed using immunohistochemistry on sections and flat-mounted retinas and western blotting on protein extracts obtained from laser microdissection of the photoreceptor layers. Semi-thin and ultrastructure analyses were also reported. Results: In the rat retina, in the subapical region zonula occludens-1 (ZO-1), junction adhesion molecule (JAM), an atypical protein kinase C, is present and the OLM shows dense labeling of occludin, JAM, and ZO-1. The presence of occludin has been confirmed using western blot analysis of the microdissected OLM region. In
Everything youll probably ever need to know about safer sex barriers, like which to use, how to use them, how to get more comfortable with them, and how surprisingly cute they are.
Everything youll probably ever need to know about safer sex barriers, like which to use, how to use them, how to get more comfortable with them, and how surprisingly cute they are.
Reliable human in vitro blood-brain barrier (BBB) models suitable for high-throughput screening are urgently needed in early drug discovery and development for assessing the ability of promising bioactive compounds to overcome the BBB. To establish an improved human in vitro BBB model, we compared four currently available and well characterized immortalized human brain capillary endothelial cell lines, hCMEC/D3, hBMEC, TY10, and BB19, with respect to barrier tightness and paracellular permeability. Co-culture systems using immortalized human astrocytes (SVG-A cell line) and immortalized human pericytes (HBPCT cell line) were designed with the aim of positively influencing barrier tightness. Tight junction (TJ) formation was assessed by transendothelial electrical resistance (TEER) measurements using a conventional epithelial voltohmmeter (EVOM) and an automated CellZscope system which records TEER and cell layer capacitance (CCL) in real-time. Paracellular permeability was assessed using two fluorescent
Approach and Results-Pregnant Sprague Dawley rats were fed LS (0.03% NaCl) or normal salt (0.3% NaCl) diets, and ischemic retinopathy was induced in the offspring. An LS diet reduced retinal neovascularization and vaso-obliteration, the mRNA and protein levels of the angiogenic factors, vascular endothelial growth factor, and erythropoietin. Microglia, which influence vascular remodeling in ischemic retinopathy, were reduced by LS as was tumor necrosis factor-α. Macroglial Müller cells maintain the integrity of the blood-retinal barrier, and in ischemic retinopathy, LS reduced their gliosis and also vascular leakage. In retina, LS reduced mineralocorticoid receptor, angiotensin type 1 receptor, and renin mRNA levels, whereas, as expected, plasma levels of aldosterone and renin were increased. The aldosterone/mineralocorticoid receptor-sensitive epithelial sodium channel alpha (ENaCα), which is expressed in Müller cells, was increased in ischemic retinopathy and reduced by LS. In cultured ...
article{1898628, abstract = {Objective: Computed tomography (CT) perfusion studies can provide valuable information regarding tumor vascularization. We report on a study assessing CT perfusion characteristics in the normal pancreas and in patients with pancreatic adenocarcinoma. Methods: Twenty healthy subjects and 20 patients with histologically confirmed pancreatic adenocarcinoma were included in the study after written informed consent and approval by our institutional review board. All subjects underwent perfusion CT imaging of the pancreas using 128-slice dual-source CT. The scanning sequence included 18 scans. Parametric maps of blood volume (BV), blood flow (BF), and permeability surface area product (PS) were generated and compared with density measurements. Results: In normal pancreas, no significant difference in perfusion values was observed between head, body, and tail of the pancreas. Mean organ values were 76.76 (SD, 15.6) mL/100 g/min, 15.80 (SD, 2.40) mL/100 g, and 27.74 (SD, ...
Symptoms of Retinal edema including 2 medical symptoms and signs of Retinal edema, alternative diagnoses, misdiagnosis, and correct diagnosis for Retinal edema signs or Retinal edema symptoms.
Macular oedema is an accumulation of fluid within the central part of the retina (the macula). This can lead to loss of the normal architecture and function of the macula causing distortion and deterioration of central vision. Macular oedema results from a breakdown in the blood-retinal barrier, with fluid accumulating both interstitially and within the retinal glial cells (Müller cells). It can occur in patients with diabetic retinopathy, retinal vein occlusions or ocular inflammation (uveitis). Macular oedema is diagnosed clinically and monitored with optical coherence tomography (Box 1, Figure 1 and Figure 2).. ...
Oxidative Medicine and Cellular Longevity is a unique peer-reviewed, Open Access journal that publishes original research and review articles dealing with the cellular and molecular mechanisms of oxidative stress in the nervous system and related organ systems in relation to aging, immune function, vascular biology, metabolism, cellular survival and cellular longevity. Oxidative stress impacts almost all acute and chronic progressive disorders and on a cellular basis is intimately linked to aging, cardiovascular disease, cancer, immune function, metabolism and neurodegeneration. The journal fills a significant void in todays scientific literature and serves as an international forum for the scientific community worldwide to translate pioneering
Acute stroke has a major effect on the cerebral vasculature with disruption of the neurovascular unit, leading to vasogenic edema. Breakdown of the blood-brain barrier (BBB) in ischemic stroke occurs in the early phases of ischemia, and is accentuated by IV treatment with recombinant tissue plasminogen activator, which increases the risk of hemorrhagic transformation and intracerebral hemorrhage.1,2 In a serendipitous observation using fluid-attenuated inversion recovery (FLAIR) MRI, gadolinium-DTPA enhancement of the CSF space overlying the ischemic tissue indicated greater stroke severity, increased age of the patient, and reperfusion injury. They called this phenomenon hyperintense acute reperfusion marker (HARM), and now Hitomi et al.3 have extended the original study to show enhancement of the structures in the eye. In addition to the endothelial blood-CNS barriers that maintain CNS homeostasis, regulate nutrition and detoxification, as well as immune cell trafficking into the brain and ...
Figure 1. Differential display analysis of TR-iBRB and TR-BBB cells. A: Typical fluorescent image of polyacrylamide gel electrophoresis. An arrow indicates selectively expressed DNA bands in TR-iBRB cells. DNA bands were cloned and sequenced. B: Nucleotide sequence of the selectively expressed clone (clone 1) marked by the arrow in A. Clone 1 sequence after nucleotide position 72 has 77% nucleotide homology with the 3 terminal of the mouse M-cadherin gene.. ...
Assessment of Blood-Brain Barrier Breakdown. Animal Models of Acute Neurological Injuries II: Injury and Mechanistic Assessments, Volume 1. 401-413. 2012 ...
Diabetes mellitus is associated with an increase in proliferative lesions in the small cerebral vessels.1 Functionally, the blood-retinal barrier is closely related to the blood-brain barrier (BBB)2 and cortical capillaries in experimental models of diabetes exhibit similar microangiopathy to that found in the human retina in diabetes.3, 4. A principal neuroradiological feature that may be associated with cerebral microvascular disease is "white matter hyperintensities" or "leukoaraiosis", a mixed condition of uncertain aetiology manifested on CT scans as hypodensity in the cerebral white matter, and as hyperintensities on T2, proton density or fluid attenuated inversion recovery (FLAIR) MR imaging.5 Recent longitudinal studies have highlighted diabetes as a risk factor for dementia, doubling the risk of senile dementia of the Alzheimer type.6 Several studies have established a correlation between the presence and extent of white matter hyperintensities and cognitive impairment, ranging from ...
Rat Retinal Microvascular Endothelial Cells from Creative Bioarray are isolated from retinal tissue of 6-8 week old laboratory Sprague-Dawley rat. Rat Retinal Microvascular Endothelial Cells are grown in T75 tissue culture flasks pre-coated with gelatin-based coating solution for 2 min and incubated in Creative Bioarray Culture Complete Growth Medium generally for 3-7 days. Cultures are then expanded. Prior to shipping, cells at passage 3 are detached from flasks and immediately cryo-preserved in vials. Each vial contains at least 1x10^6 cells per ml and is delivered frozen. The method we use to isolate endothelial cells was developed based on a combination of established and our proprietary methods. These cells are pre-coated with PECAM-1 (CD31) antibody, following the application of magnetic beads pre-coated with secondary antibody ...
Principal Investigator:Takagi Hitoshi, Project Period (FY):2014-04-01 - 2017-03-31, Research Category:Grant-in-Aid for Scientific Research (C), Section:一般, Research Field:Ophthalmology
Title:Intravitreal Steroids for the Prevention of PVR After Surgery for Retinal Detachment. VOLUME: 21 ISSUE: 32. Author(s):Caterina Gagliano, Mario D. Toro, Teresio Avitabile, Santo Stella and Maurizio G. Uva. Affiliation:Eye Clinic, University of Catania, Via Santa Sofia 78, Catania, Italy.. Keywords:Intravitreal steroids, prevention, proliferative vitreoretinopathy, retinal detachment.. Abstract:Proliferative vitreoretinopathy (PVR) can occur in eyes with rhegmatogenous retinal detachment (RRD) or after RRD surgery, and it is the most common cause of failure of this surgery, accounting for about 75% of all primary failures. Complex biological pathways induce PVR development, with growth factors and cytokines from the vitreous and from the serum (as a result of the breakdown of the blood-retinal barrier) stimulating RPE and Muller cells transformation and proliferation, and membrane formation and contraction. Identification of pre-operative risk factors, recognition of the early signs of PVR, ...
Hyperglycemia-induced inflammation causes the dysfunction of blood vessels, and Toll-like receptor 4 (TLR4) plays a key role in inflammation-induced angiogenesis. However, the impact of TLR4 on the pathogenesis of diabetic retinopathy (DR) is poorly understood. In this study, we examined the expression of TLR4 in retinal vascular endothelial cells of patients with DR and diabetic mice, and explored the role of TLR4 in mediating inflammatory responses by human microvascular endothelial cells (HMEC-1) under high-glucose condition. The expression of TLR4 in retinal vascular endothelial cells of patients with proliferative diabetic retinopathy and diabetic mice induced by streptozotocin was examined using immunofluorescence. HMEC-1 cells were cultured and the expression of TLR4, MyD88 and Interleukin-1β (IL-1β) was examined under high-glucose condition. Endothelial cells with TLR4 silencing and antagonist of TLR4 as well as endothelial cells from TLR4 deficient mice were used to study the effect of