Retinal capillary closure induced by hyperglycemia is the principal pathophysiologic abnormality underlying diabetic retinopathy, but the mechaniss by which this induction occurs are not clear. Treatment of diabetic rats for 26 weeks with aminouanidine, an inhibitor of advanced glycosylation product formation, prevented a 2.6-fold accumulation of these products at branching sites of precapillary arterioles where abnormal periodic acid/Schiff reagentpositive deposits also occurred. A dine treatment completely prevented abnormal endothelial cell proliferation and signiflcantiy diminshed pericyte dropout. After 75 weeks, untreated diabetic animals developed an 18.6-fold increase in the number of acellular capillaries and formed capillary microaneurysms, characteristic pathologic features of background diabetic retinopathy. In contrast, aminoguanidinetreated diabetic animals had only a 3.6-fold increase in acellular capillaries and no microaneurysms. These findings indicate that advanced glycosylation product accumulation contributes to the development of diabetic retinopathy and suggest that a anqidine may have future therapeutic use in this disorder.Pathologic retinal changes are found in virtually 100%o of patients having type I diabetes for 15 yr or longer (1). Underlying the complex clinical manifestations of diabetic retinopathy are two fundamental abnormalities: increased retinal vascular permeability and progressive retinal vessel closure (2, 3). Digested retinal vasculature preparations from diabetic patients and animals characteristically show early pericyte loss which is followed by acellular capillary development and microaneurysm formation (4,5). The severity of these changes is associated with the degree of chronic hyperglycemia to which the diabetic retina has been exposed, but the mechanisms by which elevated glucose levels cause retinal damage are currently not known (6, 7). Potentially important mechanisms include increased polyol pathway activity, activation of protein kinase C by de novo diacylglycerol synthesis, and altered cell/matrix functions induced by accumulated advanced glycosylation end products (8-11).Recently the nucleophilic hydrazine compound aminoguanidine has been shown to inhibit the formation of advanced glycosylation products on collagen and basement membrane both in vitro and in vivo (12,13 pepsin/0.2% HCL. After 10 min in a water bath at room temperature, the retina was subjected to digestion by 3% trypsin/0.2 M Tris for 3.5 hr at 370C to remove the inner limiting membrane. The sample was then placed on a glass slide, and further digestion with trypsin was monitored under a dissecting microscope. The intact isolated retinal vessel preparation was washed with distilled H20 and air-dried. Retinal vessel preparations were stained with periodic acid/ Schiff reagent/hematoxylin (15) and photographed using a

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Toxoplasma gondii, a parasite, has three modes of transmission: oral intake of raw or undercooked meat or contaminated fruits and vegetables, ingestion of materials contaminated with cat feces, and transplacental infection. The focus of this article is congenital toxoplasmosis, which is transmitted to the fetus across the placenta.When primary infection of the mother occurs during pregnancy, there is a 40 percent chance of fetal infection; rate of transmission and severity of infection are related to gestational age at the time of infection. The brain and retina are often affected, and there can be a wide range of clinical disease. Amniocentesis or cordocentesis provides the most accurate diagnosis.At birth, 80–90 percent of infants with congenital toxoplasmosis are asymptomatic. But further testing may reveal retinal and central nervous system abnormalities, and there is a risk of long-term sequelae. Chorioretinitis, hydrocephalus, intracranial calcifications, and convulsions are the typical presentation of classic congenital toxoplasmosis. Serology is the most common method of diagnosing neonatal infection, but more complex tests are also utilized. The prognosis for the untreated infant is poor; however, when antibiotic therapy is started early, the rate of sequelae is reduced significantly.

Arterial hypertension has been identified as a major secondary risk factor for diabetic retinopathy. However, the mechanisms by which hypertension worsens retinopathy are unknown. Inhibition of advanced glycation product formation prevents the development of experimental diabetic retinopathy in normotensive diabetic rats. In this study the effect of hypertension on the rate of diabetic retinopathy development and the formation of arteriolar thrombosis was evaluated. We also evaluated the effect of aminoguanidine, an inhibitor of advanced glycation and product formation on retinal pathology of diabetic hypertensive rats. After 26 weeks of diabetes, hypertension accelerated the development of retinopathy despite a lower mean blood glucose level than in the non-hypertensive group (diabetic spontaneous hypertensive rats (SHR) 16.00 +/- 6.83 mmol/l; diabetic normotensive Wistar Kyoto rats (WKY) 34.9 +/- 3.64 mmol/l; p < 0.0001). Diabetic SHR had nearly twice as many acellular capillaries as diabetic WKY (SHR diabetic: 91.9 +/- 7.5 acellular capillaries per mm2 of retinal area vs WKY diabetic: 53.7 +/- 8.5 acellular capillaries per mm2 of retinal area), and a 3.8-fold increase in the number of arteriolar microthromboses (SHR diabetic 23,504 +/- 5523 microns2 vs SHR non-diabetic 6228 +/- 2707 microns2). Aminoguanidine treatment of SHR diabetic rats reduced the number of acellular capillaries by 50%, and completely prevented both arteriolar deposition of PAS-positive material and abnormal microthrombus formation. These data suggest that hypertension-induced deposition of glycated proteins in the retinal vasculature plays a central role in the acceleration of diabetic retinopathy by hypertension.

A case of unilateral renal dysplasia was diagnosed in utero using realtime scanning. The diagnosis was confirmed neonatally and the affected kidney was surgically removed. Pathologic findings were consistent with the features of this malformation. The echographic characteristics of renal dysplasia and the differential diagnosis are described. The potential uses of ultrasonography in the diagnosis and follow-up of pregnancies associated with or at risk of renal malformations are discussed.