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We have developed a new method to visualize leukocytes and evaluate their kinetics in the chorioretinal microcirculation of the living eyes. Nuclear staining dyes and a scanning laser ophthalmoscope were used to image leukocytes in the fundus. Acridine orange was used to visualize leukocytes in the retinal microcirculation. For imaging leukocytes in the choroid, indocyanine green was injected intravenously. Dynamics of leukocytes in the capillaries of the retina and choroid were quantitatively estimated in monkeys and rats. This method also allowed evaluation of leukocyte-endothelial interactions, such as rolling or firm adhesion, in vivo.Acridine orange leukocyte fluography was used to study leukocyte dynamics in the following experimentally induced microcirculatory disturbances of the retina: (1) interferon-associated retinopathy, (2) ischemia-reperfusion injury of the retina, and (3) experimental diabetes mellitus.(1) Interferon-associated retinopathySystemic administration of interferon alpha enhanced leukocyte-endothelial interactions in the retina, which resulted in leukocyte rolling and entrapment in the retinal capillary beds. Leukocyte accumulation was also detected in the lung. The entrapment or accumulation of leukocytes in the microcirculation was inhibited by simultaneous administration of corticosteroids or other agents. These results suggested that leukocytes play a major role in the development of adverse effects of interferon, such as retinopathy or interstitial pneumonia.(2) Ischemia-reperfusion injury of the retinaDuring reperfusion period after transient (60 min) retinal ischemia by optic nerve ligation, the rolling of leukocytes in the retinal veins was prominent and numerous leukocytes were trapped in the retinal capillaries. The number of rolling leukocytes was at a maximum 12 hours after reperfusion. Leukocyte entrapment peaked at 24 hours after reperfusion. By blocking adhesion molecules on the vascular endothelium, these leukocyte-endothelial interactions were effectively inhibited. Postischemic retinal atrophy was also inhibited by blocking adhesion molecules. These results suggested that leukocytes may be major players in the pathophysiology of ischemia reperfusion injury of the retina.(3) Experimental diabetes mellitusLeukocyte dynamics in the retina were studied in streptozotocin-induced diabetes and spontaneous diabetes (OLETF rats). In both diabetic models, leukocyte entrapment in the retinal capillaries was increased even in the early stages of diabetes. Fluorescein angiography revealed that trapped leukocytes disturbed the regional capillary blood flow in the downstream. Enhanced expression of adhesion molecules was observed in the capillary endothelium of the retina in the diabetic rats. Leukocyte entrapment in the retinal capillaries might cause microvascular occlusions and dysfunction, in turn causing diabetic retinopathy.
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PMID:In vivo evaluation of leukocyte dynamics in the retinal and choroidal circulation 1091 67

Goshajinkigan (niu-che-shen-qi-wan in Chinese), a traditional herbal medicine, has been used in Japan to treat clinical symptoms of diabetic neuropathy. A double-masked study was performed to evaluate its effects on corneal sensitivity, superficial punctate keratopathy and tear production in patients with insulin-dependent diabetes mellitus. Fifty diabetic patients were randomized into two groups: Group A, in which 25 patients received goshajinkigan orally, 7.5 g/day for 3 months; Group B, in which 25 patients were orally administered placebo, 6.0 g/day for 3 months; and in Group C, 25 non-diabetic subjects were orally administered goshajinkigan, 7.5 g/day for 3 months. Corneal sensitivity was measured with an aesthesiometer. The area of superficial punctate keratopathy was expressed as a fluorescein staining score. Reflex tearing was determined with a Schirmer test without anesthesia goshajinkigan was analyzed by high-performance liquid chromatography. Corneal thresholds after treatment with goshajinkigan (2.03 g/mm2) in Group A were significantly lower than those before treatment (2.47 g/mm2). Those in Groups B and C did not change after treatment. Fluorescein staining scores after administration of Goshajinkigan (0.64) in Group A were significantly lower than those before treatment (1.32). Those in Groups B and C did not change after treatment. Schirmer test results after goshajinkigan administration (11.0 mm/5 min) in Group A were significantly higher than those before treatment (9.3 mm/5 min). Those in Groups B and C did not change after treatment. Hemoglobin A1c levels in Groups A, B,and C did not change after treatment. Several components in goshajinkigan were found on high performance liquid chromatography. In conclusion, goshajinkigan improved ocular surface disorders in patients with insulin-dependent diabetes mellitus.
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PMID:Effects of goshajinkigan on corneal sensitivity, superficial punctate keratopathy and tear secretion in patients with insulin-dependent diabetes mellitus. 1272 59

Diabetic maculopathy seen in the Philippines, specifically, the associated factors, the various lesions seen on fluorescein angiography, and the visual acuity associated with these lesions were characterized using 127 patients (254 eyes) with diabetic retinopathy based on the fluorescein angiography done at the Eye Referral Center in 1993. Results showed that 116 (91.34%) patients have maculopathy, the majority of which is bilateral (84.25%). Age (p=0.675), sex (p=0.357), hypertension (p=0.742), duration of diabetes (p=0.778) and myopia (p=0.742) were not significantly associated with maculopathy. However, severity of retinopathy (p=0.001) was significantly associated with it. Fluorescein angiographic findings are macular staining (83.86%), perifoveal capillary dropout or macular ischemia (10.76%), and preretinal traction and membrane (5.38%). Microaneurysm (72.65%) is the most common lesion associated with macular staining, followed by capillary leakage (4.04%), cystoid macular edema (3.59%), perifoveal capillary dropout with microaneurysm (2.24%), and capillary with microaneurysm leakage (1.34%). Exudates are associated with microaneurysm, perifoveal capillary dropout or a combination of the two. Vision was found to be marginally statistically different between the normal and maculopathy group (p=0.0505). The worst vision was seen in macular ischemia and preretinal traction and membrane, with mean visual acuity of 0.18 and 0.25, respectively. It is concluded that severity of retinopathy is the only variable significantly associated with maculopathy in this study. Good vision does not necessarily indicate a normal macula. Detailed examination and fluorescein angiography should be carried out, regardless of duration of diabetes.
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PMID:Fluorescein angiographically evident diabetic maculopathy. 1472 62

Macular edema is the final common pathway of many intraocular and systemic insults. It may develop in a diffuse pattern where the macula appears generally thickened or it may acquire the characteristic petaloid appearance referred to as cystoid macular edema. Although macular edema may be associated with protean underlying conditions, it is most commonly seen following intraocular surgery, venous occlusive disease, diabetic retinopathy, and posterior segment inflammatory disease. As well as clinical suspicion, a wide range of investigations may lead to the diagnosis of macular edema. Fluorescein angiography and optical coherence tomography provide enhanced visualization of the geometry and distribution of macular edema. A variety of approaches to the treatment of macular edema have been attempted, with a variable degree of success. These options have included topical and systemic steroids, topical and oral non-steroidal anti-inflammatory agents and laser photocoagulation treatment. More recently other therapeutic modalities, including immunomodulators, intravitreal injection of triamcinolone, and pars plana vitrectomy have also been employed. Clinical trials are currently looking into the use of a steroid slow-release intravitreal device for the management of macular edema secondary to uveitis and diabetes. This article reviews the clinical entity of macular edema focusing on the current therapeutic strategies for its management.
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PMID:Macular edema. 1532 93

The effect of lisinopril (an angiotensin-converting enzyme inhibitor) on diabetic macular edema (DME) was investigated by quantitative measurement of macular thickness. In a nonrandomized clinical trial, 19 normotensive type 2 diabetic patients with DME prospectively received oral lisinopril therapy for 2 months. Another 10 normotensive type 2 diabetic patients with similar DME were prospectively followed for two months without treatment. Central macular thickness was measured with a retinal thickness analyzer (RTA). In the lisinopril group, visual acuity improved by two lines or more in two out of 19 eyes (11%), was unchanged in 15 eyes (78%), and deteriorated by two lines or more in two eyes (11%). The mean central macular thickness was significantly reduced after 2 months of treatment (381.3 +/- 121.1 microm) compared with that before administration (475.2 +/- 171.0 microm, P = 0.0093). In the control group, central macular thickness was not significantly decreased after 2 months (458.5 +/- 113.7 microm, P = 0.2178) compared with the baseline value (464.7 +/- 152.2). Fluorescein angiography showed that macular leakage was decreased in 10 patients from the lisinopril group (53%) and was unchanged in nine patients (47%). There was a significant difference of central macular thickness between the patients with and without improvement of macular leakage (P = 0.0040). Lisinopril therapy may reduce macular thickness in patients with DME, as shown by this quantitative study. In addition, quantitative measurement of retinal thickness is useful when evaluating therapeutic agents for DME.
Diabetes Res Clin Pract 2004 Dec
PMID:Quantitative measurement of retinal thickness in patients with diabetic macular edema is useful for evaluation of therapeutic agents. 1553 18

One hundred and eight male Sprague-Dawley rats weighing 160-225 g were examined with vitreous fluorophotometry (VF). Fifty-five rats were made diabetic with streptozocin (43 with 65 mg/kg and 12 with 90 mg/kg); 53 nondiabetic rats served as controls. Fluorescein (7 mg/kg) was injected IV and VF was performed 60 min later. The diabetic rats had an abnormal blood-retinal barrier (BRB) after 4-7 days duration. The difference between the diabetic and non-diabetic rats was persistent up to 35 days (P < 0.02-0.001). The diabetic rats treated with 90 mg/kg streptozotocin had a more severe diabetes and a higher treated with 65 mg/kg (P < 0.05). The BRB function was normalized in 18 rats treated for 6-7 days with 5-6 IU long-acting insulin (P < 0.02). The results imply that streptozocin-diabetic rats have an abnormal BRB and that this abnormality seems to be related to the diabetic state and to be reversible after insulin treatment.
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PMID:Influence of metabolic control on the blood-retinal barrier in streptozocin diabetic rats. 1583 15

A 60-year-old man with diabetes mellitus had a sudden decrease in vision in his right eye 3 weeks after confirmed West Nile virus infection. Visual acuity in the right eye was 20/400. Fundus examination showed bilateral multifocal chorioretinitis, which was associated with proliferative diabetic retinopathy in the right eye and severe nonproliferative diabetic retinopathy in the left eye. There were deep, dense retinal hemorrhages, retinal opacification, and retinal arterial sheathing in the macula of the right eye. Fluorescein angiography revealed extensive capillary nonperfusion in the macular area of the right eye. Six months later, vision remained unchanged and a choroidal neovascularization developed over a chorioretinal scar in the same eye.
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PMID:Severe ischemic maculopathy in a patient with West Nile virus infection. 1674 63

Investigations of the blood-brain barrier (BBB) in diabetes have yielded contradictory results. It is possible that diabetes differentially affects paracellular and transcellular permeabilities via modulation of tight junction and transport proteins, respectively. Fluorescein (FL), a marker for paracellular permeability, is a substrate for the transport proteins organic anion transporter (OAT)-3 and multidrug resistance protein (MRP)-2 at the BBB. Furthermore, MRP-2-mediated efflux of FL can be upregulated by glucose. In this study, streptozotocin-induced diabetes led to decreased brain distribution of FL measured by in situ brain perfusion, consistent with activation of an efflux transport system for FL at the BBB. This change was paralleled by increased protein expression of MRP-2, but not OAT-3, in cerebral microvessels. These data indicate that diabetes may lead to changes in efflux transporters at the BBB and have implications for delivery of therapeutics to the central nervous system.
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PMID:Decreased blood-brain barrier permeability to fluorescein in streptozotocin-treated rats. 1711 33

Cystoid macular edema (CME) is a primary cause of reduced vision following both cataract and successful vitreoretinal surgery. The incidence of clinical CME following modern cataract surgery is 0.1-2.35%. Preexisting conditions such as diabetes mellitus and uveitis as well as intraoperative complications can raise the risk of developing CME postoperatively. The etiology of CME is not completely understood. Prolapsed or incarcerated vitreous and postoperative inflammatory processes have been proposed as causative agents. Pseudophakic CME is characterized by poor postoperative visual acuity. Fluorescein angiography is indispensable in the workup of CME, showing the classical perifoveal petaloid staining pattern and late leakage of the optic disk. Optical coherence tomography is a useful diagnostic tool, which displays cystic spaces in the outer nuclear layer. The most important differential diagnoses include age-related macular degeneration and other causes of CME such as diabetic macular edema. Most cases of pseudophakic CME resolve spontaneously. The value of prophylactic treatment is doubtful. First-line treatment of postsurgical CME should include topical nonsteroidal anti-inflammatory drugs and corticosteroids. Oral carbonic anhydrase inhibitors can be considered complementary. In cases of resistant CME, periocular or intraocular corticosteroids present an option. Antiangiogenic agents, though experimental, should be considered for nonresponsive persistent CME. Surgical options should be reserved for special indications.
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PMID:Postsurgical cystoid macular edema. 2070 48

Recent gene expression studies on mouse models for retinal degeneration identified deregulation of Pituitary tumor transforming gene 1 (Pttg1) as a potential susceptibility factor involved in photoreceptor cell death. Pttg1 is a transcription regulatory protein involved in sister chromatid segregation, and Pttg1(-/-) mice exhibit testicular and splenic hypoplasia, thymic hyperplasia, aberrant cell cycle progression, chromosome instability, and impaired glucose homeostasis leading to diabetes, particularly in older males. Due to Pttg1 deregulation in dystrophic retinas, we characterized Pttg1(-/-) retinas using Hematoxylin and Eosin (H&E) staining, immunohistochemistry (IHC), and electroretinography (ERG). Seven month old Pttg1(-/-) mice were also examined for a diabetic retinopathy phenotype using Fluorescein Angiography (FA) to test for neovascularization. Our data reveal that up to 9 months of age, Pttg1(-/-) retinas have a healthy morphology and normal photoreceptor function. This study lays the groundwork for further investigation into the relevance of Pttg1 in retinal dystrophy.
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PMID:Characterization of the pituitary tumor transforming gene 1 knockout mouse retina. 2120 37


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