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D Popov

Publications and source records attributed to D Popov.

At least 19 recordsLinked to original sources
PubMed2003

Saturated-fat diet induces moderate diabetes and severe glomerulosclerosis in hamsters.

AIMS/HYPOTHESIS: Diets high in saturated fat are thought to be a risk factor for Type 2 diabetes and associated complications. We investigated effects of a medium and high saturated fat diet on the development of diabetes-associated pathologies in Golden Syrian hamsters, an animal that reacts to dietary lipids in a fashion similar to humans. METHODS: Three diets containing 46.5 kcal %, 267.3 kcal %, and 488.2 kcal % as saturated fat respectively, were studied. Metabolic parameters were measured up to 20 weeks. Electron microscopy was used to examine the structure of the pancreas, aorta and kidney. RESULTS: Increased saturated fat consumption was associated with: (i) gradual imbalance of homeostasis, and severe structural alterations of acinar, beta cells and capillaries in the pancreas, and of the kidney glomeruli; (ii) severe hypertriglyceridaemia and augmented creatinine concentrations related to disturbances of the renal function, progressing to nodular glomerulosclerosis and nephropathy; (iii) reduced early insulin secretion in response to glucose; (iv) switch of the aortic endothelium to a secretory phenotype. CONCLUSION/INTERPRETATION: The results show that high-caloric saturated fat intake induced diabetes in hamsters, probably linked to delayed insulin secretion. The model was also associated with the development of a range of pathologies characteristic to human diabetes, including nephropathy and defects in vasculature. Thus, high-fat fed hamsters provide a new model that is likely to be useful in understanding the cellular and molecular mechanisms involved in the pathogenesis of diabetes.

Animals↗
PubMed2001

Mechanisms of decreased bradykinin- induced vasodilation in experimental hyperlipemia-hyperglycemia: contribution of nitric oxide and Ca2+-activated K+ channels.

Common complications of diabetes are accelerated atherosclerosis and vascular disturbances. We investigated whether the simultaneous insult of hyperlipemia-hyperglycemia affects the reactivity of the resistance arteries to bradykinin (BK), and if so, what are the mechanisms responsible for this disturbance. Experiments were conducted on male Golden Syrian hamsters rendered hyperlipemic (H) by a fat-rich diet, diabetic (D) by streptozotocin injection, or simultaneously hyperlipemic-diabetic (HD). Normal age-matched animals were used as controls (C). At 24 weeks after the induction of disease(s) the vascular reactivity of the mesenteric resistance arteries to BK (10(-8)-10(-4) M) was assayed by the myograph technique. To explore the role of nitric oxide (NO) in modulating the endothelium-dependent BK-induced relaxation, two experimental approaches were employed: (i) in vivo administration of L-arginine (622.14 mg/kg bw) to H, D, and HD hamsters (for 12 weeks); (ii) in vitro blockage of nitric oxide synthase by N(omega)-nitro- L-arginine methyl ester (10(-4) M). To evaluate the contribution of Ca2+-activated K+ channel(s) to BK-induced relaxation, the resistance arteries were exposed to 10(-3) M tetraethylammonium. Comparatively, the endothelium-independent relaxation was assayed using sodium nitroprusside (10(-8)-10(-4) M). The results showed that compared to the H and D groups, the HD hamsters exhibited the most reduced vasodilation of the resistance arteries to BK (34.09 +/- 1.5%). The diminished vasodilation was found to be due to a dual mechanism: an L-arginine:NO pathway and a NO-independent process, mediated via Ca2+-activated K+ channels. In vivo administration of L-arginine had favourable effects especially in the HD group, which manifested (i) an; 30% improvement of attenuated BK relaxation, (ii) an increase in sensitivity of the response to BK, (iii) a 3-fold diminishment of plasma hyperglycemia. Collectively, these data explain in part, the mechanisms and possible ways to correct the arterial endothelial dysfunction when diabetes is complicated with hyperlipemia.

Animals↗
PubMed2001

Structural and transport property alterations of the lung capillary endothelium in diabetes.

There are reports that lung function is altered in diabetes mellitus. Since data are limited concerning the structural--functional correlates in hyperglycemic animals, we designed experiments to assess: (i) whether hyperglycemia induces changes in the structure of the lung capillary endothelial cells (EC), and (ii) the effect of advanced glycation endproducts of albumin (AGE-Alb) on EC. Experiments were conducted on mice and hamsters rendered diabetics by streptozotocin (D-STZ) injection; age-matched animals were used as controls (C). The structure of EC, and the interaction of EC with AGE-Alb adsorbed to 5 nm colloidal gold (AGE-Alb.Au) were examined by electron microscopy; the uptake and cellular distribution of [125I]-AGE-Alb were investigated by spectrometry and autoradiography. The results showed that, compared to C group, in D-STZ animals the alveolar capillary EC exhibited: (i) an uneven distribution of the anionic sites exposed by the luminal plasmalemma, (ii) a metabolicaly active phenotype, (iii) a thickened basal lamina provided with focal nodules, similar in density and distribution to those found in the glomerular basal lamina in diabetes; in addition, (iv) a narrowed or collapsed lumen was found in approximately 30% of the capillaries. The functional alterations of lung EC in diabetes consisted in increased uptake of intravascularly infused [125I]-AGE-Alb and enhanced transcytosis and endocytosis of AGE-Alb.Au. The fusion of plasmalemmal vesicles, and opening of the interendothelial junctions observed, may account for the increased permeability of the alveolar capillary EC. This study asserts that hyperglycemia affects the structure and functional properties of the alveolar capillary EC, and suggests the existence of microangiopathic alterations in diabetic lung.

Animals↗
PubMed2000

Equivalence of salbutamol 200 microg four times daily propelled by propellants 11 and 12 or HFA 134a in mild to moderate asthmatics. Eastern European study group.

The phasing out of chlorofluorocarbons (CFCs) requires the development of an alternative non-ozone depleting propellant for use in pressurized metered dose inhalers (pMDIs). The present study assessed the effects on tolerability and efficacy of a switch from the currently available formulation containing the CFC propellants 11 and 12 to an alternative non-CFC formulation using the propellant hydrofluoroalkane (HFA) 134a in patients with mild to moderate asthma. After a 4-week run-in period during which patients received salbutamol 200 microg four times daily from a CFC pMDI, 547 patients were randomized to 12 weeks of treatment with salbutamol 200 microg four times daily administered from either an HFA 134a pMDI (Ventolin CFC-free; 277 patients) or CFC pMDI (Ventolin, 270 patients). At the end of this period, all patients then received a further 4 weeks of treatment with the same dose of salbutamol via a CFC pMDI (run-out period). On the basis that high doses of beta2-agonists are known to increase heart rate, change in heart rate was selected as the primary outcome variable. Small increases in heart rate were observed during the treatment period and these changes were comparable in both groups; the 90% confidence interval for the treatment differences was within the predefined limits for clinical equivalence (+/- 10 beats min(-1)). The incidence of adverse events was similar in both groups and there were no reports of paradoxical bronchospasm. Furthermore, daily PEF measurements showed comparability in terms of lung function. Symptom scores and use of additional bronchodilator were also similar in both groups. These results demonstrate that salbutamol (800 microg day(-1)), formulated with HFA 134a is equivalent to the current CFC formulation in terms of tolerability and efficacy.

Administration, Inhalation↗
PubMed2000

The effects of simultaneous hyperlipemia-hyperglycemia on the resistance arteries, myocardium and kidney glomeruli.

The experimental model of Golden Syrian hamster subjected to concomitant hyperlipemia (diet-induced) and diabetes (by streptozotocin injection) for 24 weeks is characterised by the prevalence of micro- and macroangiopathies. We have used the hyperlipemic-diabetic (HD) hamsters to investigate: a) whether there is an alteration in the reactivity of the resistance arteries (mean internal diameter: 210-250 microm), b) if present, which are the structural and biochemical changes that accompany the functional modifications, and c) to examine the pathomorphological changes induced by the association of hyperlipemia and diabetes on vital organs such as myocardium and kidney glomeruli. To these aims, biochemical assays of plasma components, light- and electronmicroscopy, myographic, morphometric and spectrofluorimetric techniques were used. The mesenteric resistance arteries of HD hamsters exhibited (as compared to similar arteries in normals) a decreased contractile response to noradrenaline (1.86+/-0.35 vs. 2.43+/-0.21), and an impeded endothelium dependent relaxation to acetylcholine (approximately 61.40% vs. approximately 79.80%). The association of hyperlipemia with diabetes induced changes in morphology of the resistance arteries consisting in approximately 10% increase of the intima plus media cross-sectional area, approximately 20% decrease of the vascular lumen area, and approximately 2.85 fold augmentation of the wall to lumen ratio. The resistance arteries exhibited structural modifications of the endothelium (up to 8 copies of Weibel-Palade bodies/endothelial cell), and smooth muscle cells (secretory phenotype), and in the vessels media small calcification cores appeared embedded in a hyperplasic extracellular matrix. The vascular mesenteric bed of the HD hamsters contained approximately 2.30 and approximately 1.30 fold increased concentrations of AGE-collagen and pentosidine, respectively, above the normal values. The HD hamsters displayed also modifications that may be dependent on or may lead to an increase in blood pressure, such as: a) approximately 2 fold increase in the activity of serum angiotensin converting enzyme; b) approximately 4.8 fold enhancement of erythrocytes fragility (as a measure of the oxidative stress); c) left ventricular hypertrophy associated with a progressive disarray of cardiomyocyte contractile fibers, interruptions of the Z bands, and accumulation of collagen-rich extracellular matrix indicative of interstitial fibrosis; d) the kidney glomerular capillaries appeared partially or totally collapsed, with a thickened basement membrane which appeared polymorphic, and in some locations made up of successive layers connected by fine bridges and intercalated nodules; in addition, an increase (approximately 1.50 fold) of the mesangial volume was indicative of glomerulosclerosis.

Acetylcholine↗
PubMed1998

Heart microvessels and aortic endothelial cells express the 15 kDa heart-type fatty acid-binding proteins.

Due to their hydrophobic nature, free fatty acids require carriers for transport across and within the cells. The endothelial layer is the first barrier to be traversed by the fatty acids, from the plasma to the underlying cells and tissues. We tried to find out whether cytosolic fatty acid-binding proteins (FABPs) are present in the endothelium of large vessels (aortic endothelial cells) and small vessels (myocardial capillaries) using the following experimental approaches: (i) loading the delipidated aortic endothelial cell (EC) homogenate and the heart cytosolic proteins and membrane proteins with [14C]palmitate or [14C]oleate, respectively, followed by autoradiographic detection of electrophoretically separated bands; (ii) detection by immunoprecipitation of heart-type FABP (H-FABP) using an affinity-purified antibody raised against bovine H-FABP (anti-H-FABP), and (iii) localization of FABP by indirect immunofluorescence and gold-immunocytochemistry applied to cultured EC and to thick and thin frozen sections of mouse heart. The results showed that: (i) within the EC homogenate proteins that express affinity for [14C]palmitate have an apparent Mr of 15000, and 40000-45000, that correspond as molecular mass to cytosolic and membrane FABPs, respectively. Similar affinity was found by incubation with [14C]oleate, that binds to a protein of Mr 15000 in the heart cytosol, and to a 40-45 kDa protein in the membrane fraction; (ii) anti-H-FABP immunoprecipitated specifically a cytosolic 15 kDa peptide (H-FABP); (iii) by indirect immunofluorescence, cytosolic H-FABP was localized on heart microvessels and myocytes and also in cultured aortic EC where intense spotted fluorescence characteristic for cytosolic antigens was present; (iv) by immunocytochemistry, H-FABP was detected in the EC cytoplasm, and in close proximity to the cytoplasmic aspect of plasmalemma and vesicle membranes. Together the data attest the presence of the 15 kDa, heart-type FABP in the endothelium of aorta and heart microvessels.

Animals↗
PubMed1998

Diabetes-induced structural changes of venous and arterial endothelium and smooth muscle cells.

The structural alterations of endothelium and smooth muscle cells of the hind limb and heart veins and arteries were investigated in Golden Syrian hamsters subjected to streptozotocin induced diabetes. Animals were examined at 5, 10, and 15 weeks after induction of diabetes. At each time point body weight and plasma glucose concentrations were recorded. Anesthetised animals were washed out of blood, fixed in situ, and the femoral vein and artery, saphenous vein and artery, and heart veins and coronaries were dissected out, and processed for electron microscopical examination. Anionic sites of the endothelial plasmalemma were visualized by in situ perfusion of cationized ferritin. The endothelial localization of von Willebrand factor was carried out by immunocytochemistry. The results showed that induction of experimental diabetes generated morphological changes of the endothelium and smooth muscle cells of both hind limb and heart vessels. The common alterations developed in endothelial cells of venous and arterial origin consisted in: 1) the development of a secretory phenotype, enriched in biosynthetic and degradative organelles; 2) the abundance of cytoskeletal elements, especially intermediary filaments; 3) the increase in number of fused plasmalemmal vesicles and transendothelial channels, and 4) the hyperplasia of the basal lamina. In contradistinction to the arterial endothelium, the peculiarities of the venous endothelium in the diabetic hamsters examined were: 1) the uniform distribution of the anionic sites exposed on the luminal plasma-lemma (as in normal animals), and 2) the increased number of copies of Weibel-Palade bodies (up to 13 copies per endothelial cell in the hind limb). Von Willebrand factor was immunodetected in Weibel-Palade bodies, Golgi cisternae and some vesicles of normal and diabetic hamsters. With time, and especially pronounced at 15 weeks of diabetes, the smooth muscle cells of veins and arteries examined exhibited a characteristic secretory phenotype, and were surrounded by a reticulated basal lamina and a hyperplasic extracellular matrix (especially pronounced in arteries). These data indicate that diabetes affects both heart and hind limb veins and arteries, producing structural changes of the endothelium and smooth muscle cells which may account, at least in part, for the specific vascular complications.

Animals↗
PubMed1997

Capillary and aortic endothelia interact in situ with nonenzymatically glycated albumin and develop specific alterations in early experimental diabetes.

Diabetic mice (6 weeks duration) were studied to assess the interaction of advanced glycation endproduct-modified albumin (AGE-Alb) with micro- and macrovascular endothelium, and to evaluate the alterations induced in the ultrastructure of the lung, kidney, and aorta. [125I]-AGE-Alb and AGE-Alb-Au were perfused in situ in the vasculature; the total uptake was quantitated by spectrometry, and the endothelial pathways of AGE-Alb-Au and the morphological alterations of the vascular beds were examined by electron microscopy. The results showed that [125I]-AGE-Alb (0.567 microM) was taken up specifically and saturably by all organs studied, and particularly by the lung. AGE-Alb-Au endocytosis and transcytosis occurred in the pulmonary and aortic endothelia, and were enhanced in diabetic animals. Also in diabetic animals, AGE-Alb-Au was detected throughout the kidney glomerular basement membrane (GBM) and within open filtration slits of podocytes, suggesting altered barrier function. The structural modifications progressed, and at the end of the experimental period, in the lung approximately 28% of the capillaries and approximately 25% of the alveoli became compressed or even collapsed, due to the hyperplasia of extracellular matrix and interstitial connective tissue. The presence of adherent intravascular macrophages suggests the development of an inflammatory immune process. The structural modifications observed in kidney glomeruli included thickening (approximately 30%) of the GBM and the disappearance of diaphragms between the cellular processes of podocytes. The aortic endothelium displayed luminal foldings, increased number (2.8-fold) of Weibel-Palade bodies, and proliferation of basal lamina. Together, the results show that in diabetes there is enhanced vascular uptake of AGE-Alb and significant pathomorphological changes of micro- and macrovessels.

Animals↗
PubMed1997

Pseudopulmonary embolism: acute respiratory distress in the syndrome of heparin-induced thrombocytopenia.

A 73-year-old man with myasthenia gravis was treated with daily plasmapheresis. During the course of treatment, the patient developed progressive thrombocytopenia and an episode of severe acute respiratory distress suggesting pulmonary embolism. The thrombocytopenia and respiratory impairment improved after discontinuation of heparin, and both recurred on heparin rechallenge. The presence of heparin-specific antibodies was confirmed by in vitro assay. The time frame of clinical events suggests a heparin-mediated mechanism for both the thrombocytopenia and respiratory compromise. We conclude that acute respiratory distress may be the presenting manifestation of the syndrome of heparin-associated thrombocytopenia in patients treated with dialysis or apheresis.

Acute Disease↗
PubMed1997

Alterations of lung structure in experimental diabetes, and diabetes associated with hyperlipidaemia in hamsters.

Since hyperglycaemia is known to affect normal pulmonary physiology and biochemistry and few structure-function correlations have been reported, we designed experiments on hamsters subjected to streptozotocin-induced diabetes or diabetes associated with hyperlipidaemia, and investigated the impact of these conditions on the lung structure. At time intervals ranging 2-24 weeks from the inception of disease (without correcting blood glucose with insulin), the animals were sacrificed, and plasma glucose and cholesterol assayed. The lung was processed for electron microscopy, and the structural changes of the capillary and venular endothelium, of epithelial cells, and interstitium were examined. In diabetic animals, especially after 6 weeks of disease, a gradual narrowing of approximately 35% of the capillaries and approximately 30% of the alveoli, and hyperplasia of the extracellular matrix, rich in collagen bundles, were observed. Frequently, capillaries contained adherent intravascular macrophages suggestive of an inflammatory process. The capillary endothelium was characterized by numerous plasmalemmal vesicles, often fused, well-developed synthesizing apparatus (endoplasmic reticulum and Golgi complex) and cytoskeleton, and an uneven distribution of the anionic sites on the luminal plasmalemma. The venular endothelium was particularly rich in Weibel-Palade bodies. The alveolar epithelium was often collapsed, compressing surfactant within the airspace. The lung interstitium was apparently enlarged, and the fibroblasts and contractile interstitial cells frequently contained lipid droplets. These alterations were more pronounced and occurred at a faster rate (4 weeks) in diabetes associated with hyperlipidaemia. The structural modifications reported in this study support the functional disturbances observed in association with hyperglycaemia, sustaining the conclusion that the lung is an organ affected by diabetes.

Animals↗
PubMed1997

Pathobiology of the heart in experimental diabetes: immunolocalization of lipoproteins, immunoglobulin G, and advanced glycation endproducts proteins in diabetic and/or hyperlipidemic hamster.

Diabetes is known to be accompanied by atherosclerotic disease and general cardiovascular complications. Hamsters were previously shown to develop hyperlipemia-induced atherosclerosis, similar in many respects to the human atherosclerotic process. To study the effect of hyperglycemia on heart vessels and valves, male Golden Syrian hamsters were rendered either diabetic or hyperlipemic and diabetic; controls were age-matched normal hamsters. At time intervals ranging from 2 to 24 weeks, animals were killed; plasma glucose, cholesterol, and lipid peroxides were measured; and the aortic arch and valves, coronary arteries, and heart microvessels were examined for ultrastructural modifications and for the presence of low-density lipoproteins (LDL), immunoglobulin G (IgG), and advanced glycation endproducts (AGE) proteins. Elevation of plasma glucose, peroxides, and cholesterol were observed in both diabetic as well as hyperlipemic and diabetic animals, along with characteristic diabetic changes: microangiopathy of the myocardium (ie, capillary narrowing, hyperplasia of basal lamina, and proliferation of extracellular matrix) and macroangiopathy of the aortic arch, valves, and coronary arteries (ie, intimal proliferation, fatty-streak formation, and calcification). LDL, IgG, and AGE-proteins were immunolocalized in focal deposits, ie, in the shoulder and cap of the plaques; these antigens were distributed diffusely in the extracellular space or within macrophage-derived foam cells and smooth muscle cells. Our findings indicate that hyperglycemia alone induces atherosclerotic lesions in the coronary arteries, aortic arch, and aortic valves as well as alterations of the extracellular matrix of heart microvessels and cardiomyocytes, changes which together may lead to cardiomyopathy, a common and severe complication of diabetes. In addition, the present study suggests that when hyperglycemia is accompanied by hyperlipemia, detectable amounts of modified LDL (possibly oxidized or glycated) and AGE are present in the intima of atherosclerotic arteries; and also that modified lipoproteins can act as immunoactive components of the atheroscerotic process generated by hyperglycemia.

Animals↗
PubMed1996

The pathomorphological alterations of endocardial endothelium in experimental diabetes and diabetes associated with hyperlipidemia.

The structural alterations of endocardial endothelial cells of the heart right atrium and left ventricle were investigated in Golden Syrian hamsters subjected to streptozotocin-induced diabetes and to a combination of diabetes and diet-induced hyperlipidemia. Animals were examined at time intervals ranging from 2 weeks to 6 months. Anionic sites of the endothelial plasmalemma were visualized by in situ perfusion of cationized ferritin. The results indicated that: (a) both atrial and ventricular endocardial endothelium are affected in streptozotocin-induced diabetes: endothelium converts from continuous into a fenestrated type, (b) although the anionic charge of the plasmalemma decreased in advanced diabetes, the newly formed fenestrae highly bound cationized ferritin, (c) combined diabetes and hyperlipidemia induced more severe alterations of endocardial endothelium: new permeable endothelial structures were formed (transendothelial channels, open intercellular junctions, fused plasmalemmal vesicles), and the cells became particularly enriched in cytoskeleton (intermediate filaments and microtubules), (d) the thick subendocardial layer of connective tissue contained, in the combined experimental model, macrophage derived foam cells indicative for the occurrence of alterations of atherosclerotic type.

Animals↗
PubMed1996

Pathobiochemistry of combined diabetes and atherosclerosis studied on a novel animal model. The hyperlipemic-hyperglycemic hamster.

Because accelerated atherosclerosis is the main complication of diabetes, we devised a new animal model that combines these two diseases, and investigated their joint impact on the main plasma components and organs known to be most affected in each disorder. Male Golden Syrian hamsters were subjected to three experimental conditions: streptozotocin-induced diabetes (D), diet-induced hyperlipemia (H), and a combination of hyperlipemia and diabetes (HD). At time intervals ranging from 2 to 24 weeks, the animals were sacrificed, the appropriate plasma constituents were determined, and the ultrastructural modifications of relevant tissues such as the heart, cardiac valves, coronary arteries, aorta, retina, and kidney were examined. The HD hamsters were characterized by marked alternations of plasma components, ie, increase in circulating glucose, cholesterol and lipid peroxide levels, glycation of albumin, and the appearance of irreversibly glycated albumin (AGE-Alb). These humoral changes coexisted with micro- and macroangiopathic lesions characteristic to both diseases, ie, capillary narrowing, hyperplasia of endothelial basal lamina, proliferation of perivascular extracellular matrix (abnormalities reminiscent of type I diabetes), and concomitant intimal accumulation of modified lipoproteins and macrophage-derived foam cells in the aorta, coronaries, and cardiac valves, leading to accelerated formation of atherosclerotic plaques. These changes eventually appeared in the D hamsters also, but at a much slower rate, whereas the H group showed only modifications characteristic for atherosclerosis. Our findings indicate that, overall, 1) diabetes accelerated the early development and progression of atherosclerotic lesions leading to rapid calcification, and 2) hyperlipidemia associated with diabetes accelerated the rate of development of diabetes-induced microvascular disease. The hamster model may be useful to study the impact of various drugs on the diabetes-related vascular complications.

Animals↗
PubMed1994

Receptor for advanced glycation end products (AGEs) has a central role in vessel wall interactions and gene activation in response to circulating AGE proteins.

The extended interaction of aldoses with proteins or lipids results in nonenzymatic glycation and oxidation, ultimately forming AGEs, the presence of which in the plasma and vessel wall is associated with diabetic vascular complications. We show here that AGE albumin in the intravascular space interacts with the vessel wall via binding to an integral membrane protein, receptor for AGE (RAGE), a member of the immunoglobulin superfamily, resulting in clearance from the plasma and induction of interleukin 6 mRNA. Intravenously infused 125I-AGE albumin showed a rapid phase of plasma clearance with deposition in several organs. Rapid removal of 125I-AGE albumin from the plasma was prevented by administration of a soluble, truncated form of RAGE, which blocked binding of 125I-labeled AGE albumin to cultured endothelial cells and mononuclear phagocytes, as well as by pretreatment with anti-RAGE IgG. Ultrastructural studies with AGE albumin-colloidal gold conjugates perfused in situ showed that in murine coronary vasculature this probe was taken up by endothelial plasmalemmal vesicles followed by transport either to the abluminal surface or by accumulation in intracellular vesicular structures reminiscent of endosomes and lysosomes. Consequences of AGE-RAGE interaction included induction of interleukin 6 mRNA expression in mice. These data indicate that RAGE mediates the interaction of AGEs with the vessel wall, both for removal of these glycated proteins from the plasma and for changes in gene expression.

Animals↗
PubMed1993

Multi-aperture viewing: perception of figures through very small apertures.

A new phenomenon of viewing objects through multiple apertures is reported. When a solid figure is hidden behind a sieve of very small apertures (pinholes), only its general shape may be perceived. Outline figures may be entirely invisible behind the sieve. Motion of the figure markedly improves the visibility of the outline figures and of the small details and edges of the solid figures. Two experiments are presented. The first demonstrates that the size of a dark stimulus moving behind a rear-illuminated row of holes is perceived with an accuracy that may be considerably better (i.e. the error is smaller) than the interhole distance. The results of the second experiment show that the visibility of an outline figure, a ring, is significantly better when the figure smoothly moves than when presented at random positions behind a two-dimensional sieve. Changing the velocity within the range of 5.18-10.36 deg/sec does not affect the visibility of the figure while it moves; however, a lower rate of discrete presentation leads to significantly better visibility. An explanation of the phenomenon is presented in terms of integration of information about the relative positions of the covered/uncovered holes, with a possible involvement of motion analyzing mechanisms.

Adult↗