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Biomedical subjects

A Takeuchi

Publications and source records attributed to A Takeuchi.

At least 523 records · Page 29Linked to original sources
PubMed1976

Electron microscope studies of experimental Entamoeba histolytica infection in the guinea pig. II. Early cellular and vascular changes accompanying invasion of the lamina propria.

Early cellular and vascular changes in response to invasion of lamina propria by Entamoeba histolytica were studied sequentially, at the ultrastructural level, in germfree guinea pigs inoculated intracecally with amebae and enteric flora derived from patients with acute amebic colitis. Approximately one week post-inoculation the animals developed acute colitis with mucosal invasion by trophic amebae. Although epithelial cells at the sites of amebic invasion showed progressive cytoplasmic changes and desquamation resulting in microerosions, most mesenchymal elements in the lamina propria appeared normal without cytopathic changes even when in direct contact with invading amebae. Only the polymorpho-nuclear leukocytes (PMN) apposed or topographically close to amebae exhibited degenerative changes which were characterized by condensation of nucleoplasm and cytoplasm, extra-cellular release of cytoplasmic components including granules, and, finally, lysis of cell membranes. Capillaries and venules in the lamina propria showed a variety of changes such as swelling and gap formation at the intercellular endothelial junctions and more rarely at the fenestrae. Blood vessels physically close to amebae showed formation of endothelial cytoplasmic blebs which pinched off into the vascular or extravascular space. Platelet and fibrin thromboses were common in the more severely damaged capillaries and venules. Fragments or clumps of fibrin-like material were found also in the extracellular spaces. Amebic invasion of the lamina propria, then, is accompanied by continued epithelial shedding, PMN degeneration, and changes in both capillaries and venules consisting of endothelial damage and occlusive thrombosis. The vascular changes appeared to be closely related to PMN degeneration resulting from interaction of PMN with invading amebae.

Amebiasis↗
PubMed1976

Freeze-etching observations of trophozoites of pathogenic Entamoeba histolytica.

Pathogenic Entamoeba histolytica trophozoites were studied by the freeze-etching (FE) technique of electron microscopy. Surface replicas of intact cell membranes were highly convoluted with numerous invaginations, evaginations, and undulations. Sperical depressions and elevations varying from 0.5 mu to 1.0 mu in diameter were commonly present on the external cell membrane and appeared to represent an extracellular secretory mechanism of trophozoites. Cleaved surfaces of amebae exhibited a granular and lumpy cytoplasm in which there were many vesicles and vacuoles that ranged in diameter from 0.2 mu to 9.0 mu. Some vacuoles contained tightly enveloped bacteria, while others contained bacteria and host cytocomponents. Occasional vesicles and vacuoles appeared to be fused to each other. Replicas of FE nucleus were enclosed by double nuclear membranes which were fenestrated by numerous sperical pores measuring approximately 640 A in diameter and spaced at intervals of 650 A. Counts of nuclear pores were possible and indicated 35 pores per square micron on the nuclear envelope. Golgi apparatus, mitochondria and well formed endoplasmic reticulum were absent in FE replicas. This was in agreement with electron microscope observations on thin sections previously reported by other investigators.

Animals↗
PubMed1976

Studies on the pathogenesis of enteric infections caused by invasive bacteria.

Salmonellae, shigellae and some Escherichia coli must invade the intestinal epithelial cell and multiply within the mucosa to cause disease. Although the bacterial cell most likely possesses several properties essential to this invasive ability, the nature of the cell envelope complex is at present the only characteristic which has been implicated in this process. While a number of pathophysiological events result from invasion, some of our recent efforts have concerned the site and mechanism of intestinal fluid loss in salmonellosis and shigellosis. In both these disorders, bacterial invasion of the colonic mucosa, associated with an acute inflammatory reaction and mucosal damage, is regularly seen and colonic salt and water transport is abnormal. These defects may account for mild diarrhoea in salmonellosis and the dysenteric stools of shigellosis. However, in salmonella-infected animals with severe watery diarrhoea and in shigella-infected animals with diarrhoea alone or in combination with dysentery, the jejunum is in a net secretory state. This secretion occurs in the absence of bacterial invasion or morphological abnormalities. Thus, the diarrhoea caused by invasive bacteria may result from the inability of the colon to reabsorb the increased volume of fluid entering it from the small intestine. Although colonic mucosal damage is a feature of invasive-type diarrhoeas, the permeability of both the colon and small intestine to small molecules, mannitol and erythritol, is not altered. Thus intestinal fluid loss cannot be ascribed to transudation. In addition, the results of our Ussing chamber experiments, employing salmonella-infected rabbit ileum, reveal that salt and water secretion is an active process. Since secretion occurs in the jejunum in the absence of bacterial invasion, this might suggest the participation of an enterotoxin. Shigella dysenteriae I is the best-studied invasive organism in which an enterotoxin has been found, yet mutant strains which do not invade but retain the ability to elaborate enterotoxin fail to cause disease in either monkeys or man. Thus, the physiological relevance of Shiga enterotoxin and the mechanism of jejunal secretion in these disorders remain unclear. Recent data suggest that invasive enteropathogens, like the enterotoxin-producing bacteria, activate the mucosal adenylate cyclase-cyclic AMP system and that this activation may play a role in intestinal fluid secretion.

Animals↗
PubMed1976

Permeability changes produced by L-glutamate at the excitatory post-synaptic membrane of the crayfish muscle.

1. Permeability changes produced by L-glutamate at the neuromuscular junction of the crayfish (Cambarus clarkii) were investigated by application of the drug iontophoretically to the voltage-clamped junction and measuring the resulting 'glutamate current'. 2. Reversal potentials were determined by measuring the glutamate current at different membrane potentials. They were +39-1 +/- 3-6 mV (mean +/- S.E. of mean) in normal solution and +16-5 +/- 2-0 mV in solutions made twice as hypertonic by the addition of sucrose. 3. Decreasing external Na+ concentration shifted the reversal potential in the negative direction; increased Na+ in the positive direction. 4. The relation between the amplitude of the glutamate current and extracellular Na+ concentration was approximately linear. 5. Alteration of the external K+ or Cl- concentration did not affect the amplitude or reversal potential of glutamate current. 6. In Na+-free solution the application of L-glutamate produced a small inward current at the resting potential and its amplitude was augmented by increasing the external Ca2+ concentration. 7. Increasing the Ca2+ concentration in the normal Na+ media produced no appreciable effect on the reversal potential but decreased the amplitude of glutamate current. 8. The results indicate that L-glutamate increases the membrane permeability mainly to Na+ and slightly to Ca2+. 9. The time course of glutamate current was shorter than that of the concentration calculated from the diffusion equation and it was simulated more closely by the square of the concentration.

Animals↗
PubMed1976

Electron microscope study of experimental enteric adenovirus infection in mice.

Using fluorescent antibody techniques (FA) and light microscopy (LM) and electron microscopy (EM), this paper describes the morphological features of the ileum in the DK1 mouse orally challenged with adenovirus K87. At the peak of infection, virus is easily identified by FA in the epithelium of the villi and crypts of the ileum. LM shows that fluorescent cells have large, bizarre, uniformly basophilic nuclei containing deoxyribonucleic acid, as indicated by histochemical tests. EM further identifies these nuclei as belonging to columnar, goblet, or Paneth cells, all epithelial cells facing the lumen with a microvillus border. The basophilic material in the nuclei consists of virus particles 75 nm in diameter arranged in crystalline arrays. When found in the cell cytoplasm, the virions do not form arrays but are scattered or form irregular aggregates, which may or may not be enclosed by single membranes. Infected columnar cells show mild cytopathic effects with no cell degeneration and necrosis, whereas the goblet and Paneth cells appear normal and maintain synthetic and secretory functions. All infected cells, however, share an abnormally accelerated extrusion rate, with columnar and goblet cells often being shed from the side rather than from the tip of the villi. The Paneth cells, which do not migrate out of the crypts, show a higher than normal rate of extrusion in the crypt lumen.

Adenoviridae↗
PubMed1976

Electron microscope study of experimental enteric infection in neonatal dogs with a canine coronavirus.

Neonatal dogs, inoculated orally with coronavirus 1-71, grown in canine kidney cell cultures, developed diarrhea and a severe enteritis characterized by atrophy of the villi, changes in the enterocytes, and accelerated epithelial cell loss. Electron microscopy of the mucosal epithelium, 4 days after challenge, showed that the virus penetrated into the enterocytes between microvilli, possibly by pinocytotic mechanism. In the enterocytes, virions were most often enclosed, singly or in groups, in cytoplasmic vesicles. They were less frequently found in the cisternae of the Golgi apparatus, the endoplasmic reticulum, or in the dilated perinuclear space and only rarely, free in the cytoplasm. Virions replicated by budding only on the smooth.membranes of the cytoplasmic vesicles. The infected cells showed a variety of cytopathic effects, some nonspecific, such as disruption of the microvilli, loss of density of the cytoplasm, presence of lipid inclusions, alteration of mitochondria, and dilation of the endoplasmic reticulum and Golgi cisternae and of the perinuclear space. Other cytopathic effects, characteristic of the coronavirus infection, consisted of formation of dense filamentous structures and of membrane-bound bodies. Progeny virions appeared to discharge into the gut lumen through the disrupted cell membranes of infected enterocytes still in situ or following their premature shedding.

Animals↗
PubMed1975

Ionic mechanism of the excitatory synaptic membrane of the crayfish neuromuscular junction.

1. The reversal potential for the excitatory neuromuscular junction of the crayfish (Cambarus clarkii) was measured using the voltage clamp method. The potential change was recorded with an intracellular microcapillary and the negative phase of the output of the feed-back amplifier was connected to the stainless-steel wire which was inserted longitudinally into the muscle fibre. 2. When the excitatory nerve was stimulated, a transient feed-back current flowed inwardly through the membrane. This current was called the excitatory junctional current (e.j.c.). 3. Reversal potentials were determined by extrapolating the e.j.c.s measured at different membrane potentials. They were about 10-20 mV positive with respect to the bath solution (11-5 +/- 1-2 mV, mean +/- S.E.). 4. The reversal potential for the iontophoretically applied glutamate was identical with that for the e.j.c. 5. In hypertonic solutions, the reversal potentials for e.j.c. and glutamate became more negative. 6. When the sodium concentration of the bath solution was decreased, the reversal potential became more negative. 7. When the chloride and potassium concentration were altered, little, if any, change was observed in the reversal potential. 8. It was concluded that the e.j.c. was carried mainly by sodium ions. Contribution of other ions, possibly calcium ions, was discussed.

Animals↗
PubMed1975

Pheochromocytoma with renal artery stenosis and high plasma renin activity.

An unusual case of pheochromocytoma is described in this communication. Besides a chain of typical clinical pictures and laboratory findings which suggested a catecholamine-producing tumor, the left renal artery stenosis was demonstrated by an aortography and the plasma renin activity was consistently elevated. Surgery revealed the left renal artery was embedded in the tumor mass, originated from the left adrenal gland, resulting in a high degree of constricture of the vessel. Following the removal of the tumor, blood pressure immediately returned to normal, however, plasma renin activity remained elevated as long as 9 months of the follow-up study. The second aortography performed 14 months after the operation failed to demonstrate the left renal artery stenosis and subsequent studies revealed that plasma renin activity was gradually declining to upper normal levels. It is suggested that an excess of catecholamines secreted by the tumor was responsible for hypertension in this case, and that another factor, probably renal artery stenosis, was involved in the elevation of plasma renin activity, although this high renin activity was maintained for more than 9 months following the tumor extirpation.

Adolescent↗
PubMed1975

Electron microscope studies of experimental Entamoeba histolytica infection in the guinea pig. I. Penetration of the intestinal epithelium by trophozoites.

Germ-free guinea pigs were inoculated intracecally with Entamoeba histolytica and the enteric flora derived from a human patient with acute amebic colitis. Aanimals were killed at post-inoculation intervals of 7 to 12 days. The mode of penetration of cecal epithelium by the ameba was examined by light and electron microscopy. The following sequence was reconstructed from numerous individual observations. When the amebae were in moderately close proximity to the brush, border, the microvilli became shortened, irregular, and sometimes disappeared. Dense material was observed between the amebae and microvilli. When the ameba was very close to the epithelium the apical portion of epithelial cytoplasm projected into the lumen contacting the organism, thus becoming detached from adjoining cells. This produced spaces between epithelial cells through which amebae invaded interepithelial spaces. Initially the ameba penetrated the interglandular epithelium. Later, it penetrated equally the glandular and interglandular epithelium barrier. There were marked alterations of cytoplasmic components of epithelial cells. Polymorphonuclear leukocytes migrated into the epithelium filling these spaces; these often showed a variety of degenerative processes. Amebae, utilizing their pseudopodia, moved further through the intercellular spaces and reached the lamina propria.

Animals↗
PubMed1975

Small intestinal mucosal injury in the experimental blind loop syndrome. Light- and electron-microscopic and histochemical studies.

Microscopic (light and electron) and histochemical abnormalities have been demonstrated in the jejunum of rats with the blind loop syndrome. Three groups of animals were studied: normal control animals, and animals with either self-filling (SF) or self-emptying (SE) blind loops. Vitamin B12 malabsorption and bacterial overgrowth occurred only in those animals with SF blind loops. Three jejunal segments were studied: the blind loop segment and the jejunal segments proximal and distal to the blind loop. In the animals with the blind loop syndrome, those with SF blind loops, the most striking findings occurred in the blind loop itself, with similar but less marked changes in the jejunum distal but not proximal to the blind loop segment. Hypertrophy of both crypts and villi was evident with focal abnormalities of villus architecture. Approximately 10 to 20% of the columnar cells in the upper half of the villi were swollen and vesiculated. By electron microscopy microvilli demonstrated a variety of degeneration changes and the glycocalyx and terminal web were disrupted. Mitochondria and endoplasmic reticulum (ER), both smooth and rough, were swollen. Concentric whorls of parallel membranes and long, curvilinear rough ER were present in the cytoplasm. Histochemically, there was loss of enzymatic activity in the epithelial brush border, mitochondria and ER. Inasmuch as bacterial invasion of the jejunal mucosa was not seen, the etiology of these changes is not known but may involve bacterial "toxins" or products of bacterial metabolism. These morphological observations demonstrate that both brush border and intracellular injury occur in the jejunal epithelial cell of rats with the experimental blind loop syndrome.

Animals↗