Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0344329 (collapse)
 28,634 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In LLC-PK1 cells exposed to patulin (50 microM), lipid peroxidation, abrupt calcium influx, extensive blebbing, and total LDH release appeared to be serially connected events with each representing a step in the loss of structural integrity of the plasma membrane. The aforementioned patulin-induced events were prevented by concurrent incubation with butylated hydroxytoluene, deferoxamine, and cyclopiazonic acid, a fungal metabolite. Patulin also caused depletion of nonprotein sulfhydryls, increased 86Rb+ efflux, dome collapse, and eventually the loss of cell viability. These events were not prevented by antioxidants, results consistent with the hypothesis that they were also serially connected but occurring parallel to those previously mentioned. The earliest events observed in patulin-treated cells were the decrease in nonprotein sulfhydryls and increase in 86Rb+ efflux (5 min) which occurred before statistically significant alterations in protein-bound sulfhydryls. The increased potassium efflux (86Rb+ efflux) occurred via a pathway distinct from BaCl2, quinine, or tetraethylammonium sensitive potassium channels. This is the first published report of the antioxidant activity of indole tetramic acids (cyclopiazonic acid and cyclopiazonic acid imine). The protective effect of tetramic acids in LLC-PK1 cells was restricted to indole tetramic acids, and their prevention of lipid peroxidation did not involve iron chelation. The results of this study demonstrate that cyclopiazonic acid is a potent inhibitor of azide-insensitive, ATP-dependent, a23187-sensitive calcium uptake by the lysate of LLC-PK1 cells. This result is consistent with the hypothesis that the endoplasmic reticulum calcium transport ATPase is a sensitive target for cyclopiazonic acid in LLC-PK1 cells. These findings raise the interesting possibility that the antioxidant activity of indole tetramic acids may involve multiple novel mechanisms: surface charge alterations on the cytoplasmic surface of plasma membranes, alterations in calcium permeability in the plasma and endoplasmic reticulum membrane, and inhibition of the calcium-dependent ATPase of the endoplasmic reticulum.
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PMID:The mechanism of patulin's cytotoxicity and the antioxidant activity of indole tetramic acids. 203 42

Rhinosporidium seeberi, the causative organism of rhinosporidiosis of the nasal mucosa and skin was reviewed with regard to its pathogenesis and histopathology, histochemistry, ultrastructure, life cycle, and cultivation. The pathological findings from infected tissues reveal a granulomatous reaction comprising mixed cell granuloma, pseudocystic abscesses, fibrosis around the causative organism (R. seeberi), and transepidermal elimination. The cell walls of trophocytes and sporangia exhibit the presence of cellulose. The spore wall is encapsulated with granular fibrillary substances consisting of acid mucopolysaccharides. Spheroid bodies have proved to be DNA surrounded by a thin membrane-bound layer. In the cytoplasm of the organism, various substances can be detected by histochemical methods (e.g., glycogen, glycoprotein, acid mucopolysaccharides, neutral lipids, and phospholipids). The walls of the sporangia are found to be trilaminated, whereas those of trophocytes are bilaminated. There is a myriad of curvilinear structures around the outer wall of both forms. The ultrastructure of a trophocyte shows it to be comprised of sporoblasts containing oval or round membrane-bound nuclei with nucleoli, mitochondria, endoplasmic reticulum, chromatin granules, vacuoles, lipid bodies, and spherules. We suggest that the multilamellar bodies are precursors of trophocytes and sporangia. Abortive trophocytes without cytoplasmic organelles are seen, and they collapse at the end of the maturation process. Rhinosporidium seeberi fails to grow in any of the artificial media used but can be maintained through its life cycle in tissue cultures.
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PMID:Rhinosporidiosis. 268 23

Ultrastructural changes were observed in 23 consecutive patients who died from fulminant hepatic failure due to hepatitis B virus (4 cases), sporadic non-A, non-B (7), or paracetamol (acetaminophen) overdose (12) and in 3 patients with subacute hepatic necrosis of unknown cause. The findings are described in detail in 12 of these patients. Fatal fulminant hepatitis was characterised by massive confluent necrosis accompanied by collapse of reticulin framework and sudden drop-out of liver cells. No aetiological distinction could be made between different viral causes of fulminant hepatitis on the basis of ultrastructural pathology. Parenchymal changes in viral cases varied from reversible non-specific necrosis to irreversible changes where fragmentation of endoplasmic reticulum, mitochondria and nuclei had occurred. Differences in ultrastructural pathology between non-viral (paracetamol overdose-induced) and viral fulminant hepatitis were apparent. Modification of endoplasmic reticulum with enlarged attached polyribosomes, breakdown of plasma membrane, accumulation of cytoplasmic amorphous material and karyorrhexis and karyolysis of nuclei were the most prominent features in non-viral cases.
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PMID:Fulminant hepatitis. An ultrastructural study. 308 70

We have used plant root tips frozen under high pressure in conjunction with freeze-fracture electron microscopy a) to evaluate the quality of freezing of unfixed, non-cryoprotected tissues obtainable with this method, b) to examine the structure of cells frozen under high pressure, c) to evaluate the usefulness of high pressure freezing to preserve transient membrane events, and d) to look for artifacts caused by the high pressure. A single artifact of high pressure, possibly related to the collapse of air spaces during pressurization before freezing, manifested itself as long tears or folds in the plasma membrane. Excellent freezing, as evidenced by the smooth, turgid appearance of all membrane systems and the lack of aggregated cytosolic materials was observed in 10 to 20% of samples. In the best preserved specimens freezing was uniform throughout the sample volume and all organelles were readily identified. In the remaining ones, a gradient of ice crystal sizes was seen; cells within 50 to 100 microns of the surface being better preserved than those in the interior. Cortical microtubules appeared well preserved as were close associations of endoplasmic reticulum (ER) with nuclear, Golgi and plasma membranes. Junctions between the ER and nuclear membrane were constricted and much thinner (30 nm in diameter) than in chemically-fixed, thin-sectioned tissue, and although no continuities between the ER and Golgi membranes were observed, many Golgi stacks had an adjacent ER cisterna either at the cis or trans face. Both Golgi and ER cisternae exhibited distinct, round dilations indicative of vesicle blebbing or vesicle fusion events. Characteristic disc- and horseshoe-shaped infoldings of the plasma membrane corresponding to fused secretory vesicle and/or membrane recycling structures were also prominent in many cells. Short extensions of the cortical ER cisternae were regularly observed appressed against these plasma membrane infoldings suggesting a functional role for the ER in vesicle-mediated secretion and/or membrane recycling. Many lipid bodies were intimately associated with the ER, some with their surface monolayer fused with the cytoplasmic leaflet of the ER membrane. Our findings demonstrate that high pressure freezing can provide excellent morphological preservation of intact tissues and can preserve fast, transient membrane events such as those associated with vesicle fusion and vesicle blebbing. We conclude that this is the best available method for freezing relatively large (up to 0.6 mm thick) tissue samples for study by electron microscopy.
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PMID:High pressure freezing of intact plant tissues. Evaluation and characterization of novel features of the endoplasmic reticulum and associated membrane systems. 339 90

The membranes of Acanthamoeba palestinensis were studied by examination in fixed cells, and then by following the movements of glycerol-(3)H-labeled phospholipids by cell fractionation. Two previously undescribed structures were observed: collapsed cytoplasmic vesicles of cup shape, and plaques in food vacuole and plasma membrane similar in size to the collapsed vesicles. It appeared that the plaques formed by insertion of collapsed vesicles into membranes and/or that collapsed vesicles formed by pinching off of plaques. Fractions were isolated, enriched with nuclei, rough endoplasmic reticulum (RER), plasma membrane, Golgi-like membranes, and collapsed vesicles. The changes in specific activity of glycerol-(3)H-labeled phospholipids in these membranes during incorporation, turnover, and after pulse-labeling indicated an ordered sequence of appearances of newly synthesized phospholipids, first in nuclei and RER, then successively in Golgi membranes, collapsed vesicles, and finally, plasma membrane. In previous work we had found no large nonmembranous phospholipid pool in A. palestinensis. These observations are consistent with the hypothesis that membrane phospholipids are synthesized, perhaps as integral parts of membranes, in RER and nuclei. Subsequently, some of the newly synthesized phospholipids are transported to the Golgi complex to become integrated into the membranes of collapsed vesicles, which are precursors of the plasma membrane. Collapsed vesicles from the plasma membrane by inserting into it as plaques. When portions of the plasmalemma from food vacuoles, collapsed vesicles pinch off from their membranes and are recycled back to the cell surface.
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PMID:Assembly of lipids into membranes in Acanthamoeba palestinensis. II. The origin and fate of glycerol- 3 H--labeled phospholipids of cellular membranes. 432 52

A study was carried out to assess the effects of prostaglandin(PG)E2 on the fine structure of human luteal tissue in vitro. The laboratory procedures are explained and microscopic photographs of the results are included. Biopsies of corpora lutea from 4 normal women at 10-16 weeks gestation were incubated in a buffer medium containing acetate-C and 20-40 mcg/ml of PGE2 for 3 hours. Preincubation and incubation controls and the PGE2-treated samples from each of the 4 biopsies were studied by electron microscopy. In all cases, the controls were well preserved and the luteal cells had the fine structural characteristics previously described in early pregnancy. The morphologic changes which occurred in the human luteal cells incubated in PGE2 solution varied from cell to cell in each sample. The changes were remarkable, indicating cell damage. Main changes were: collapse and disarrangement of the smooth endoplasmic reticulum, ballooning or condensation of mitochondria, disappearance of the rough endoplasmic reticulum, dilatation and/or disappearance of the Golgi system, accumulation of lipid droplets, and increased lysosomes. The results also indicate that not only the synthesis of progesterone is impeded, but more significantly, the de novo synthesis of cholesterol from incorporation of acetate may be severely impaired. Findings in this study contradict the results of several earlier studies. This study shows a direct luteolytic effect of PGE2 in vitro.
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PMID:Ultrastructural changes of the human corpus luteum of pregnancy induced by prostaglandin E2 in vitro. 447 20

Light microscopic and electron microscopic findings in thymuses from 4-week old feline leukemia virus-infected and 4- and 9-week old noninfected kittens were evaluated and found to be morphologically similar to each other. Thymuses from 9-week old feline leukemia virusinfected kittens were markedly atrophied and individual lobules within each thymus varied in the severity of atrophy. Loubules having the least severe atrophy had a moderate thinning of the cortex and a heterogeneous thymuses included intense eosinopoiesis at the corticomedullary junction, increased prominence of vasculature, and enlarged Hassal's corpuscles. In addition to these changes lobules of thymus having the most severe atrophy had a marked cortical thymocyte depletion, lobule collapse, and increased numbers of mast cells. Degeneration of epithelial cells in most lobules was indicated by electronlucency of the cytoplasmic matrix and often greatly dilated rough endoplasmic reticulum.
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PMID:Light and electron microscopic evaluation of thymuses from feline leukemia virus-infected kittens. 624 86

The present ultrastructural morphometric study was performed to examine the mechanism of prolactin (PRL) secretion in lactating rats, compared with the alteration in serum and pituitary PRL as measured by radioimmunoassay. After 8 hours separation from pups, the pituitary PRL content double but serum PRL levels dropped markedly, whereas, in PRL cells, the granule content increased and dilated rough endoplasmic reticulum (RER) was observed. Until 30 min. after renewed suckling, a marked increase in the serum PRL was observed and the RER transformed frequently, ie. collapse (1, 30 min.) and dilation (5, 15 min.). However, the pituitary PRL and the granule content did not change noticeably. Between 60 and 240 min. after the renewed suckling, the serum PRL decreased gradually, and the pituitary PRL and the granule content showed a prominent decrease. However, the dilated RER and the well-developed Golgi apparatus were clearly observed. The results indicate that: The interrupted suckling stimulus does not suppress de novo synthesis of PRL. Renewed suckling immediately induces not only release but also de novo synthesis of PRL. Until 30 min. after renewed suckling, PRL is mainly released directly from RER, which mechanism is differently from the release by exocytosis of secretory granules that can be observed after 30 min. of renewed suckling.
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PMID:[Ultrastructural morphometric method for the measurement of prolactin release and synthesis in the rat pituitary induced by suckling stimulus]. 641 86

The Clara cells are a group of cells, sometimes called "nonciliated bronchiolar secretory cells", found in the bronchiolar epithelium of mammals including man, and in the upper airways of some species such as mice. Their secretory function is assumed from their ultrastructural appearance, that usually includes copious smooth endoplasmic reticulum, many apical mitochondria and scanty secretory-like dense vesicles near the luminal membrane. An apical cap of the cell usually bulges into the airway lumen, and secretion may be by shedding this cap, or by diffusion secretion or by merocrine secretion in individual granules. The chemical nature of the secretion probably includes protein, glycoprotein and lipids. The secretion may contain enzymes. Its function is presumably to determine the chemical and physical properties of the lining of small airways, and it could behave as a kind of bronchiolar surfactant, limiting lung collapse. The Clara cells also contain much cytochrome P450 dependent mixed-function oxidases, which presumably play a detoxifying role. It is not known whether these oxidases can be secreted or whether they have a lipid-synthesizing function. Clara cells may be important in human disease, both by giving rise to tumours and by taking part in metaplastic changes in bronchiolar disease.
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PMID:The Clara cell. 704 86

Golgi complex beads are 10-nm particles arranged in rings on the smooth surface of rough endoplasmic reticulum (ER) makind the forming face of the Golgi complex (GC). In arthropod cells they stain specifically with bismuth. Their morphology has been studied after treatment with reagents known to interfere with GC function. Inhibitors of oxidative phosphorylation (antimycin A, cyanide, and anoxia), but not an inhibitor of glycolysis (iodoacetate), both cause the bead rings to collapse and the GC saccules to round up, and inhibit transition vesicle (TV) formation. Cycloheximide blocks protein synthesis on ribosomes but does not stop TV formation or disrupt bead rings, even after prolonged treatment (6 h) to allow emptying of the rough ER cisternae. Thus the collapse of bead rings is not attributable to inhibition of protein synthesis, and the ring structure of beads does not require continued protein synthesis and secretion for its maintenance. Valinomycin has effects on the GC similar to those of antimycin A, but A23187, monensin, and lasalocid do not affect bead ring structure or TV formation. These results are consistent with valinomycin's secondarily uncoupling mitochondria, which collapses bead rings and prevents TV formation. Thus inhibitors of oxidative phosphorylation do not influence the beads through cation movement. Because mononsin and lasalocid block secretion at the level of the condensing vacuoles, bead rings are not influenced by blocks in secretion distal to them or by the backup of secretory material. These experiments are consistent with inhibitors of oxidative phosphorylation collapsing bead rings by decreasing intracellular ATP. The concomitant block to TV formation and the collapse of bead rings suggests that integrity of the bead rings is essential for the transport of secretory material from the rough ER to the GC.
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PMID:Bead rings at the endoplasmic reticulum-Golgi complex boundary: morphological changes accompanying inhibition of intracellular transport of secretory proteins in arthropod fat body tissue. 725 78


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