Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The behavior of membranes concerned with parathyroid hormone secretion was studied by electron microscopic morphometry in parathyroid cells of rats with temporarily reduced serum calcium concentration resulting from phosphate ion application and in rats with elevated serum calcium concentration following vitamin D3 administration. The phosphate ion application resulted in an increase of the cell surface area and a concomitant decrease of the surface area of the Golgi complex and secretory granules within 3 hours. After 3 hours, the cell surface area decreased, whereas the surface area of the Golgi complex and the secretory granules increased, and after 12 hours, the surface area of the rough endoplasmic reticulum also increased. In the vitamin D3-treated rats the surface area of the secretory granules increased, but the cell surface area had decreased by 24, 48, and 72 hours after application. These data suggest that parathyroid cells respond to a transient depression of the serum calcium concentration by an initial centrifugal membrane shift indicating enhanced exocytosis, followed by a centripedal membrane shift indicating enhanced endocytic retrieval of the plasma membrane. Later, membrane synthesis led to an increase of the membrane compartments concerned with parathyroid hormone secretion. Elevation of the serum calcium concentration following vitamin D3 treatment resulted in reduced release of parathyroid hormone by exocytosis and enhanced retrieval of plasma membranes by endocytosis. The fate of the retrieval plasma membrane remains unclear.
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PMID:Quantitative aspects of membrane behavior in rat parathyroid cells after depression or elevation of serum calcium. 388 31

Ultrastructural changes were followed in Plasmodium berghei after the treatment of the mouse host with a single 10 mg kg-1 dose of artemisinine (qinghaosu). After 30 minutes, changes in the limiting and other membranes of the parasite were seen, together with alterations in ribosomal organization and endoplasmic reticulum. No changes were noted in digestive vacuoles or pigment, but nuclear membrane blebbing developed after one hour and segregation of the nucleoplasm after three hours. Further degenerative changes with disorganization and death occurred from eight hours onwards. The morphological changes in ribosomes and endoplasmic reticulum correlate in time with the depression in protein synthesis observed in P. falciparum in vitro. Similarly, the onset of nucleoplasmic segregation correlates with the development of nucleic acid synthesis inhibition. Tritiated reduced drug was shown to be localized in parasite membranes, indicating that changes in membrane integrity might precede the early depression of protein synthesis. Membrane association of artemisinine may be related to its amphipathic characteristics and similarity in some respects to a sterol.
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PMID:The chemotherapy of rodent malaria, XXXIX. Ultrastructural changes following treatment with artemisinine of Plasmodium berghei infection in mice, with observations of the localization of [3H]-dihydroartemisinine in P. falciparum in vitro. 390 56

The morphogenesis and repair of airway and alveolar injury induced by bovine respiratory syncytial virus (BRSV) was studied ultrastructurally in conventional calves to characterize pulmonary cell types susceptible to viral infection and cytopathologic changes associated with infection. Viral nucleocapsids and budding virions were present in tracheal and bronchial ciliated and nonciliated epithelial cells and mucous cells 3, 5, and 7 days after inoculation and in bronchiolar ciliated and nonciliated epithelial cells 5 days after inoculation. Mild interstitial pneumonia was observed 5 days after inoculation and was characterized by swelling of type 1 and type 2 alveolar epithelial cells, interstitial edema, and infiltration by lymphocytes and macrophages. Viral assembly and release in tracheal and bronchial epithelial cells was associated with loss of cilia from ciliated cells, formation of syncytial epithelial cells, swelling of mitochondria and endoplasmic reticulum, and cell necrosis. Neutrophils, lymphocytes, and macrophages were present in close association with the viral-infected and damaged epithelial cells. There was intercurrent hyperplasia of basal epithelial cells that, in association with other epithelial lesions, resulted in the loss of normal ciliated epithelium in these airways 5 and 7 days after inoculation. Regeneration of airway epithelium was largely completed by 10 days after inoculation, except in 1 of 4 calves that had failure of epithelial repair and that developed secondary bacterial pneumonia. Pulmonary ultrastructure in BRSV-inoculated calves 30 days after inoculation was indistinguishable from that in controls. The results demonstrated that BRSV can induce reversible alterations in airway epithelium, which may cause depression of mucociliary clearance and thereby enhance susceptibility to bacterial infection.
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PMID:Experimental bovine respiratory syncytial virus infection in conventional calves: ultrastructural respiratory lesions. 399 22

Rats given a single subdermal injection into the left hind paw of 0.5 mg Mycobacterium tuberculosis suspended in 0.1 ml of mineral oil, after several days of latency, developed arthritis accompanied by depression in liver microsomal phosphatidylcholine and phosphatidylethanolamine synthesis at 7, 14 and 21 days. The depression of liver microsomal phosphatidylcholine and phosphatidylethanolamine concentrations of experimental animals was accompanied by decreased incorporation of radioactive palmitate into both phospholipids. Nevertheless, the biosynthesis of phosphatidylcholine via the methylation pathway was unaffected. These observations suggest that adjuvant arthritis affects quantitatively the phospholipid composition of the liver endoplasmic reticulum, which consequently may lead to impairment of the microsomal drug-metabolizing enzyme system.
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PMID:The effect of adjuvant-induced arthritis on rat liver microsomal phospholipid metabolism. 407 96

We studied the influence of prolonged exposure to hyperoxia (O(2) > 98%) on protein synthesis and on the ultrastructure of the granular pneumocyte. To study protein synthesis, as indicated by l-[U-(14)C]-leucine incorporation into protein, lung slices were incubated with radioactive leucine and a surface-active fraction was obtained by ultracentrifugation of lung homogenates. We found that, following an initial depression in protein synthesis after 48 h of hyperoxia, protein synthesis in rats exposed to oxygen for 96 h rose to greater than control levels. This increase in protein synthesis was noted in whole lung protein and in protein present in the surface-active fraction. Stereologic ultrastructural analysis of granular pneumocytes revealed that the lamellar bodies occupy the same percentage of cytoplasmic volume in oxygen-exposed and control rats after 96 h; a previous study had shown lamellar bodies of oxygen-exposed rats to occupy less volume than those of control rats after 48 h of exposure at which time protein synthesis was also depressed. After 96 h of exposure there is a greater amount of rough endoplasmic reticulum in the granular pneumocytes of oxygen-exposed rats. These studies show that after 96 h of hyperoxia the lung has recovered its ability to synthesize protein including protein in the surface-active fraction and that these biochemical changes are associated with consistent ultrastructural alterations in the granular pneumocyte.
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PMID:Adaption to hyperoxia. Influence on protein synthesis by lung and on granular pneumocyte ultrastructure. 440 5

Incubation of neuronal cell bodies in a calcium-free medium depresses the amount, but not the rate, of fast axonal transport of [3H]protein. Under these conditions, which do not affect protein synthesis or general energy metabolism, less protein appears to be loaded onto the transport system. Depression of transport also is seen when cell bodies are exposed to medium containing Co2+; selective exposure of axons to this medium has no effect on transport. These findings have led to the concept of an initiation phase of fast axonal transport that comprises the events by which selected proteins are transferred from their polysomal sites of synthesis to the transport system. The divalent cation specificity of the Ca2+ requirement, and its occurrence subsequent to Golgi apparatus-associated glycosylation, suggest that proteins destined for fast axonal transport are routed through the soma in a manner similar to that of secretory proteins and integral membrane proteins in nonneural cells. This analogy is pursued to consider a scheme whereby Golgi-derived vesicles deliver fast-transported proteins to the axonal smooth endoplasmic reticulum. Possible roles of Ca2+ in the formation and exocytotic fusion of such vesicles are considered.
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PMID:The role of calcium in the initiation of fast axonal transport. 615 71

The secretory activity of parathyroid glands in rats was stimulated by decreasing the serum Ca++ concentration through constant intravenous infusion of EGTA. The morphometric analysis of the nuclear and cytoplasmic volume and of the surface area of the rough endoplasmic reticulum, Golgi complex, secretory granules and plasma membrane revealed a membrane shift from secretory granules and Golgi complex to the plasma membrane within 1 hr of calcium depression. Subsequently, between 1 and 3 hr of calcium depression, the membrane shift was from the plasma membrane to the Golgi complex. It is considered likely that these membrane shifts are related to a rise in release of parathyroid hormone by exocytosis and a subsequent increase in retrieval of plasma membrane by endocytosis--probably through the compartment of coated pits and coated and uncoated vesicles.
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PMID:Quantitative aspects of membrane shifts in rat parathyroid cells initiated by decrease in serum calcium. 623 79

To study the possible hepatotoxicity of vitamin A supplementation and its potentiation by ethanol, rats were fed diets with either normal or fivefold increased vitamin A content, both with or without ethanol. Ethanol with a normal vitamin A diet produced the expected proliferation of the smooth endoplasmic reticulum and moderate mitochondrial lesions. Vitamin A supplementation by itself produced endoplasmic reticulum proliferation, slight enlargement of mitochondria, and moderate decrease in cytochrome oxidase activity and cytochrome aa3 content. The combination of high vitamin A and ethanol resulted in much more striking lesions, with giant mitochondria containing paracrystalline inclusions and depression of oxygen consumption in state-3 respiration with five different substrates, including palmitate and palmitoyl coA. The depression of fatty acid oxidation may have contributed to the lipid accumulation. The blood levels of vitamin A were unaffected whereas liver levels of vitamin A were increased by vitamin A supplementation and decreased by ethanol. As a net result the liver vitamin A content of the high-A-ethanol groups was not greater than that of the normal-A-control group, suggesting that a metabolite of vitamin A rather than vitamin A itself may have been responsible for the potentiation of vitamin A toxicity by ethanol. Mitochondrial toxicity reflected itself also in decreased content of various cytochromes and reduced activity of enzymes, including glutamate dehydrogenase. The activity of the latter was increased in the serum. Implications of these findings for the routine treatment of alcoholics with vitamin A and the monitoring for possible signs of toxicity are discussed.
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PMID:Hepatotoxicity of vitamin A and ethanol in the rat. 627 29

Eleven patients with moderate drug-induced liver changes were found to have extremely low hepatic vitamin A levels (less than 10% of normal). Their serum vitamin A, retinol-binding protein, and transthyretin were only slightly affected. In rats, two representative drugs (phenobarbital and methylcholanthrene) produced a significant depression of hepatic vitamin A, whereas plasma vitamin A levels remained normal. The livers of drug-treated animals showed no abnormalities except for the expected proliferation of the smooth endoplasmic reticulum and induction of microsomal enzymes and cytochrome P-450 (phenobarbital) and P-448 (methylcholanthrene). These findings suggest that the decrease in hepatic vitamin A may be secondary, at least in part, to enhanced microsomal metabolism.
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PMID:Decreased hepatic vitamin A after drug administration in men and in rats. 650 38

Macrophage numbers increased in the spleen, liver, testes, heart, and kidney of deer mice infected for seven to ten weeks with Trypanosoma brucei EATRO 110. The macrophages were activated as indicated by their increased size and significant increases in numbers of cell organelles including profiles of rough endoplasmic reticulum (which also increased in length), mitochondria, primary and secondary lysosomes, bundles of Golgi's apparatus, and free lysosomes compared to macrophages from control mice. Some macrophages representing epithelioid cells have even greater numbers of organelles than the activated macrophages and had interdigitation in some locations, such as the heart, but with minimal phagocytic activity. These epithelioid cells were present in the kidney, testes, and particularly in the heart of infected mice. Few cardiac macrophages had finely granular deposits on their nuclear membrane. The activated macrophages had enhanced phagocytosis of trypanosomes, red blood cells, neutrophils, eosinophils, lymphocytes, and plasma cells. In addition to phagocytosis, another probable consequence of macrophage activation may be depression of lymphocyte function. Phagocytosis of trypanosomes by neutrophils also was encountered occasionally.
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PMID:Pathogenesis of Trypanosoma brucei infection in deer mice (Peromyscus maniculatus). V. Macrophage ultrastructure and function. 663 69


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