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Query: UMLS:C0344329 (collapse)
 28,634 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A West Highland white terrier was evaluated because of persistent hypoglycemia and an acute episode of collapse. A pancreatic insulin-secreting neoplasm (insulinoma) was diagnosed on the basis of clinical signs, serum glucose levels, serum insulin levels, abdominal ultrasonography, and exploratory laparotomy with histologic evaluation of neoplastic tissue.
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PMID:Pancreatic insulin-secreting neoplasm (insulinoma) in a West Highland white terrier. 1034 97

The mechanism involved in N-methyl-D-glucamine (NMDA)-induced Ca(2+)-dependent intracellular acidosis is not clear. In this study, we investigated in detail several possible mechanisms using cultured rat cerebellar granule cells and microfluorometry [fura 2-AM or 2', 7'-bis(2-carboxyethyl)-5(6)-carboxyfluorescein-AM]. When 100 microM NMDA or 40 mM KCl was added, a marked increase in the intracellular Ca(2+) concentration ([Ca(2+)](i)) and a decrease in the intracellular pH were seen. Acidosis was completely prevented by the use of Ca(2+)-free medium or 1,2-bis(2-aminophenoxy)ethane-N,N,N', N'-tetraacetic acid-AM, suggesting that it resulted from an influx of extracellular Ca(2+). The following four mechanisms that could conceivably have been involved were excluded: 1) Ca(2+) displacement of intracellular H(+) from common binding sites; 2) activation of an acid loader or inhibition of acid extruders; 3) overproduction of CO(2) or lactate; and 4) collapse of the mitochondrial membrane potential due to Ca(2+) uptake, resulting in inhibition of cytosolic H(+) uptake. However, NMDA/KCl-induced acidosis was largely prevented by glycolytic inhibitors (iodoacetate or deoxyglucose in glucose-free medium) or by inhibitors of the Ca(2+)-ATPase (i.e., Ca(2+)/H(+) exchanger), including La(3+), orthovanadate, eosin B, or an extracellular pH of 8.5. Our results therefore suggest that Ca(2+)-ATPase is involved in NMDA-induced intracellular acidosis in granule cells. We also provide new evidence that NMDA-evoked intracellular acidosis probably serves as a negative feedback signal, probably with the acidification itself inhibiting the NMDA-induced [Ca(2+)](i) increase.
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PMID:Novel role of the Ca(2+)-ATPase in NMDA-induced intracellular acidification. 1051 2

Small-deformation rotational oscillation was used to examine the effect of small additions of galactomannan and kappa-carrageenan on the vitrification of glucose syrup at a total level of solids of 83%. The method of reduced variables allowed construction of composite curves covering the glass transition and glassy state (from 10(5) to 10(9.5) Pa) over a wide frequency range (up to 15 orders of magnitude). The combined WLF/free volume framework was employed to determine the rheological glass transition temperature (T(g)), fractional free volume and thermal expansion coefficient of the samples. It was found that the WLF-predicted glass transition temperature matched the cross over of experimental modulus traces in the passage from the glass transition (GG') to the glassy state (GG"). This coincides with the mechanistic transformation from free volume effects to the Arrhenius-type phenomena, thus ascribing physical significance to the rheological T(g). The T(g) value of 83% glucose syrup at a scan rate of 2 degrees C min(-1) was -25.3 degrees C. Replacing, for example, 1% glucose syrup with guar gum shifted the T(g) of the mixture to -19.7 degrees C. Network formation via the K(+)-supported junction zones of the kappa-carrageenan chains further increased the T(g) to about -1 degrees C. It appears that the low rates of relaxation processes and diffusion mobility in the presence of a polysaccharide network accelerate the collapse of the free volume thus inducing vitrification of the high sugar/polysaccharide mixture at high temperatures.
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PMID:Viscous solutions, networks and the glass transition in high sugar galactomannan and kappa-carrageenan mixtures. 1070 81

Normal cardiac function requires a tight interaction between metabolism, contractile function and gene expression. The main perturbation challenging this equilibrium in vivo is ischemia, which alters energy flux through the control of key enzymes. The review highlights metabolic imprints and energetic aspects of programmed cell survival, programmed cell death, and of necrosis. When sustained and severe, ischemia leads to a total collapse of energy transfer, to the accumulation of metabolic endproducts, and to the development of myocardial necrosis. When moderate, ischemia results in a coordinated cellular response including enhanced anaerobic glucose metabolism, a modification of cardiac gene expression, and the development of specific mechanisms for programmed cell survival (preconditioning, stunning, hibernation). Repetitive stress results in a decrease of contractile function, a downregulation of gene expression and an impairment of energy transfer, which eventually cause the heart to fail. When the failing heart becomes energy-depleted, the programs of cell survival are no longer operational and programmed cell death ensues. To define the point of departure from programmed cell survival to cell death remains a major challenge.
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PMID:Metabolic aspects of programmed cell survival and cell death in the heart. 1072 75

The purpose of this work was to analyse in vivo the influence of sudden oxygen depletion on Saccharomyces cerevisiae, grown in glucose-limited chemostat culture, using a recently developed cyclone reactor coupled with (31)P NMR spectroscopy. Before, during and after the transition, intracellular and extracellular phosphorylated metabolites as well as the pHs in the different cellular compartments were monitored with a time resolution of 2.5 min. The employed integrated NMR bioreactor system allowed the defined glucose-limited continuous cultivation of yeast at a density of 75 g DW/l and a p(O(2)) of 30% air saturation. A purely oxidative metabolism was maintained at all times. In vivo (31)P NMR spectra obtained were of excellent quality and even allowed the detection of phosphoenolpyruvate (PEP). During the switch from aerobic to anaerobic conditions, a rapid, significant decrease of intracellular ATP and PEP levels was observed and the cytoplasmic pH decreased from 7.5 to 6.8. This change, which was accompanied by a transient influx of extracellular inorganic phosphate (P(i)), appeared to correlate linearly with the decrease of the ATP concentration, suggesting that the cause of the partial collapse of the plasma membrane pH gradient was a reduced availability of ATP. The complete phosphorous balance established from our measurement data showed that polyphosphate was not the source of the increased intracellular P(i). The derived intracellular P(i), ATP and ADP concentration data confirmed that the glycolytic flux at the level of glyceraldehyde-3-phosphate dehydrogenase, 3-phosphoglycerate kinase and enolase enzymes is mainly controlled by thermodynamic constraints.
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PMID:Dynamic in vivo (31)P nuclear magnetic resonance study of Saccharomyces cerevisiae in glucose-limited chemostat culture during the aerobic-anaerobic shift. 1079 Jun 85

Aggressively growing tumors are highly dependent on the blood glucose supply. Whenever the blood glucose supply is high they grow rapidly and whenever the blood glucose supply is low they grow slowly. In cases of bonafide reports of spontaneous remissions and regressions of cancer, this tumor regulatory mechanism fails and the tumor grows rapidly and steadily despite a low blood glucose supply. This results in the collapse of the tumor system and its removal by the immune system. In lay language, it can be compared to a car that can be driven safely at 60 mph, but if it is driven at 200 mph, it will turn over and stop. Accelerated tumor growth can be induced in many ways such as: (a) reducing tumor mass which will result in a compensatory tumor growth; (b) administering hormones; (c) increasing body temperature; (d) reducing blood cortisol level; and (e) temporarily suppressing cellular immunity. A simple example would be a case of a patient with advanced and widespread cancer. If the tumor mass is reduced at once it will result in compensatory tumor growth and if hypoglycemia is initiated just prior to reducing the tumor mass and the hypoglycemia is maintained, it could possibly be followed with a brief tumor growth and the remission of cancer. The suggested procedure has not been tested or proven to be correct as yet; it is not recommended unless done under careful supervision.
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PMID:A hypothesis on the biochemistry of spontaneous remissions of cancer: coupling of oxidative phosphorylation and the remission of cancer. 1085 Mar 15

The mitochondrion is a key organelle in the control of cell death. Nitric oxide (NO) inhibits complex IV in the respiratory chain and is reported to possess both proapoptotic and antiapoptotic actions. We investigated the effects of continuous inhibition of respiration by NO on mitochondrial energy status and cell viability. Serum-deprived human T cell leukemia (Jurkat) cells were exposed to NO at a concentration that caused continuous and complete (approximately 85%) inhibition of respiration. Serum deprivation caused progressive loss of mitochondrial membrane potential (Deltapsi(m)) and apoptotic cell death. In the presence of NO, Deltapsi(m) was maintained compared to controls, and cells were protected from apoptosis. Similar results were obtained by using staurosporin as the apoptotic stimulus. As exposure of serum-deprived cells to NO progressed (>5 h), however, Deltapsi(m) fell, correlating with the appearance of early apoptotic features and a decrease in cell viability. Glucose deprivation or iodoacetate treatment of cells in the presence of NO resulted in a collapse of Deltapsi(m), demonstrating involvement of glycolytic ATP in its maintenance. Under these conditions cell viability also was decreased. Treatment with oligomycin and/or bongkrekic acid indicated that the maintenance of Deltapsi(m) during exposure to NO is caused by reversal of the ATP synthase and other electrogenic pumps. Thus, blockade of complex IV by NO initiates a protective action in the mitochondrion to maintain Deltapsi(m) this results in prevention of apoptosis. It is likely that during cellular stress involving increased generation of NO this compound will trigger a similar sequence of events, depending on its concentration and duration of release.
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PMID:The effect of nitric oxide on cell respiration: A key to understanding its role in cell survival or death. 1112 Oct 62

Adenosine (ADO) is a well-known regulator of a variety of physiological functions in the heart. In stress conditions, like hypoxia or ischemia, the concentration of adenosine in the extracellular fluid rises dramatically, mainly through the breakdown of ATP. The degradation of adenosine in the ischemic myocytes induced damage in these cells, but it may simultaneously exert protective effects in the heart by activation of the adenosine receptors. The contribution of ADO to stimulation of protective effects was reported in human and animal hearts, but not in rat hearts. The aim of this study was to evaluate the role of adenosine A1 and A3 receptors (A1R and A3R), in protection of isolated cardiac myocytes of newborn rats from ischemic injury. The hypoxic conditions were simulated by exposure of cultured rat cardiomyocytes (4-5 days in vitro), to an atmosphere of a N2 (95%) and CO2 (5%) mixture, in glucose-free medium for 90 min. The cardiotoxic and cardioprotective effects of ADO ligands were measured by the release of lactate dehydrogenase (LDH) into the medium. Morphological investigation includes immunohistochemistry, image analysis of living and fixed cells and electron microscopy were executed. Pretreatment with the adenosine deaminase considerably increased the hypoxic damage in the cardiomyocytes indicating the importance of extracellular adenosine. Blocking adenosine receptors with selective A1 and A3 receptor antagonists abolished the protective effects of adenosine. A1R and A3R activation during the hypoxic insult delays onset of irreversible cell injury and collapse of mitochondrial membrane potential as assessed using DASPMI fluorochrom. Cardioprotection induced by the A1R agonist, CCPA, was abolished by an A1R antagonist, DPCPX, and was not affected by an A3R antagonist, MRS 1523. Cardioprotection caused by the A3R agonist, Cl-IB-MECA, was antagonized completely by MRS 1523 and only partially by DPCPX. Activation of both A1R and A3R together was more efficient in protection against hypoxia than by each one alone. Our study indicates that activation of either A1 or A3 adenosine receptors in the rat can attenuate myocyte injury during hypoxia. Highly selective A1R and A3R agonists may have potential as cardioprotective agents against ischemia or heart surgery.
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PMID:Cardioprotective effects of adenosine A1 and A3 receptor activation during hypoxia in isolated rat cardiac myocytes. 1126 59

To evaluate the participation of mitochondrial damage, oxygen radicals and cell death in diabetes mellitus, we designed a way to investigate INS-1 cells, rat pancreatic beta-cell line, to die by treatment with alloxan which generate reactive oxygen species (ROS). Incubation of INS-1 cells with alloxan for 24 h resulted in a decrease in viability of cells as well as inhibition of glucose-stimulated insulin release; this could be prevented by antioxidants, vitamin E and butylated hydroxyanisol (BHA). The formation of a DNA ladder and the distribution of phosphatidylserine at the external surface of plasma membrane were observed as indicators of apoptosis in the cells treated with alloxan at concentrations below 0.5 mM. The formation of DNA ladder was prevented by vitamin E, BHA and catalase, suggesting that the ROS is involved in the process of apoptosis in INS-1 cells treated with alloxan. Lower levels of intracellular ATP, collapse of mitochondrial membrane potential and release of cytochrome c from mitochondria were also observed in INS-1 cells treated with alloxan, suggesting that alloxan caused the damage of mitochondria in cells and was related to the process of apoptosis. In contrast, rat liver RLC-18 cells treated with alloxan were not observed in the decrease of viability. It follows from the present study that mitochondrial damages by ROS generated from alloxan is linked to apoptosis in INS-1 cells.
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PMID:Apoptosis and mitochondrial damage in INS-1 cells treated with alloxan. 1151 Apr 77

Flavoproteins can function as hydrophobic sites for vitamin B(2) (riboflavin) or, in other structures, with cofactors for catalytic reactions such as glucose oxidation. In this contribution, we report direct observation of charge separation and recombination in two flavoproteins: riboflavin-binding protein and glucose oxidase. With femtosecond resolution, we observed the ultrafast electron transfer from tryptophan(s) to riboflavin in the riboflavin-binding protein, with two reaction times: approximately 100 fs (86% component) and 700 fs (14%). The charge recombination was observed to take place in 8 ps, as probed by the decay of the charge-separated state and the recovery of the ground state. The time scale for charge separation and recombination indicates the local structural tightness for the dynamics to occur that fast and with efficiency of more than 99%. In contrast, in glucose oxidase, electron transfer between flavin-adenine-dinucleotide and tryptophan(s)/tyrosine(s) takes much longer times, 1.8 ps (75%) and 10 ps (25%); the corresponding charge recombination occurs on two time scales, 30 ps and nanoseconds, and the efficiency is still more than 97%. The contrast in time scales for the two structurally different proteins (of the same family) correlates with the distinction in function: hydrophobic recognition of the vitamin in the former requires a tightly bound structure (ultrafast dynamics), and oxidation-reduction reactions in the latter prefer the formation of a charge-separated state that lives long enough for chemistry to occur efficiently. Finally, we also studied the influence on the dynamics of protein conformations at different ionic strengths and denaturant concentrations and observed the sharp collapse of the hydrophobic cleft and, in contrast, the gradual change of glucose oxidase.
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PMID:Femtosecond dynamics of flavoproteins: charge separation and recombination in riboflavine (vitamin B2)-binding protein and in glucose oxidase enzyme. 1159 97


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