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| 2. |
- Drakenberg, Torbjörn, et al.
(författare)
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Calcium Ion Binding to Pancreatic Phospholipase A2 and Its Zymogen : A 43Ca NMR Study
- 1984
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Ingår i: Biochemistry. - : American Chemical Society (ACS). - 0006-2960 .- 1520-4995. ; 23:11, s. 2387-2392
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Tidskriftsartikel (refereegranskat)abstract
- Calcium ion binding to phospholipase A2 and its zymogen has been studied by 43Ca NMR. The temperature dependence of the band shape of the calcium-43 NMR signal has been used to calculate the calcium ion exchange rate. The on-rate was calculated to be 5 × 106 M-1 s-1, which is 2 orders of magnitude less than the diffusion limit of the hydrated Ca2+ ion in water. The 43Ca quadrupole coupling constant for calcium ions bound to phospholipase, χ = 1.4 MHz, is significantly larger than those found for EF-hand proteins, indicating a less symmetric site. For prophospholipase A2, we found χ = 0.8 MHz, indicating a calcium binding site, which is somewhat more symmetric than the EF-hand sites. The dependence of the Ca NMR band shape on the calcium ion concentration showed that there are two cation binding sites on the phospholipase A2 molecule: K1 = 4 × 103 M-1 and K2 = 20 M. The strong site was found to be affected by a pKa = 6.5 and the weak site by pKa = 4.5.
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| 3. |
- Hougaard, Kjeld, et al.
(författare)
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Cerebral metabolic and circulatory effects of 1,1,1-trichloroethane, a neurotoxic industrial solvent - 1. Effects on local cerebral glucose consumption and blood flow during acute exposure
- 1984
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Ingår i: Neurochemical Pathology. - 0734-600X. ; 2:1, s. 39-53
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Tidskriftsartikel (refereegranskat)abstract
- The effects of inhaled 1,1,1-trichloroethane (3500, 6000, and 7800 ppm) on behavior, local cerebral blood flow, and local cerebral glucose consumption were studied in awake rats. The effect of the solvent inhalation on the EEG pattern and local cerebral blood flow was also studied in paralyzed animals under N2O analgesia. Exposure of awake animals to 6000 ppm 1,1,1-trichloroethane induced a decrease in motility and exploratory behavior. At 7800 ppm the rats were clearly ataxic. The local cerebral glucose consumption in 23 brain regions was studied by the [14C]deoxyglucose technique. A decrease was observed ranging from 14 to 55% of control values. The inferior colliculus and substantia nigra displayed the largest reductions. In exposed animals the local cerebral blood flow increased in 11 brain structures by 28-45%. In animals under N2O analgesia, 7400 ppm 1,1,1-trichloroethane induced a depression of the EEG activity. In these animals the local cerebral blood flow increased by 12-99%, with a large variability in blood flow between the different structures. It is concluded that exposure of rats to subanesthetic doses of 1,1,1-trichloroethane induces an increase in cerebral blood flow in spite of a concomitant decrease in glucose consumption and depression of cerebral function.
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| 5. |
- Lindman, Björn, et al.
(författare)
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Aggregation, aggregate composition, and dynamics in aqueous sodium cholate solutions
- 1980
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Ingår i: Journal of Colloid and Interface Science. - : Elsevier BV. - 0021-9797. ; 73:2, s. 556-565
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Tidskriftsartikel (refereegranskat)abstract
- The translational mobility of aggregates formed in aqueous sodium cholate solutions was obtained from the self-diffusion coefficient of solubilized decanol, which was determined using the capillary tube method with radioactive labeling. Combining these results with the self-diffusion coefficients of cholate ions, sodium ions, and water molecules the following quantities were determined as a function of cholate concentration: the fraction of cholate aggregated, the ratio of counterions and cholate ions in the aggregates, and the hydration number of the aggregates. All the quantities considered differ in their concentration dependences from those of typical micelle forming long chain ionic surfactants. There seems to be no distinctly favored aggregate size but rather the aggregate radius and aggregation number increase progressively with increasing concentration. The aggregation number is much smaller than for typical surfactant micelles. The deduced fraction of aggregated cholate shows that association progresses continuously over a wide concentration range without a well-defined critical micelle concentration. Sodium ion binding to cholate aggregates is highly variable with a rapid increase taking place above 0.1 mole/kg, a conclusion which may also be drawn from 23Na chemical shift and relaxation data. The counterion binding is discussed in relation to the so-called ion condensation model, found to apply with good approximation for simple surfactant aggregates, and in relation to the progressive cholate aggregation. The aggregates are rather strongly hydrated and the hydration number shows a peculiar concentration dependence. Information on the orientation of cholate within the aggregates is deduced by combining deuterium NMR relaxation data of deuterated cholate with the diffusion results. The order parameter is rather insensitive to concentration and points to a packing of cholate in the aggregates which does not change appreciably with concentration and which corresponds to a marked mobility of cholate within the aggregates.
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| 6. |
- Smith, Maj‐Lis ‐L, et al.
(författare)
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Models for studying long‐term recovery following forebrain ischemia in the rat. 2. A 2‐vessel occlusion model
- 1984
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Ingår i: Acta Neurologica Scandinavica. - : Hindawi Limited. - 0001-6314 .- 1600-0404. ; 69:6, s. 385-401
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Forskningsöversikt (refereegranskat)abstract
- ABSTRACT— A model is described in which transient ischemia is induced in rats anaesthetized with N2O:O2 (70:30) by bilateral carotid artery clamping combined with a lowering of mean arterial blood pressure to 50 mm Hg, the latter being achieved by bleeding, or by bleeding supplemented with administration of trimetaphan or phentolamine. By the use of intubation, muscle paralysis with suxamethonium chloride, and insertion of tail arterial and venous catheters, it was possible to induce reversible ischemia for long‐term recovery studies. Autoradiographic measurements of local CBF showed that the procedure reduced CBF in neocortical areas, hippocampus, and caudoputamen to near‐zero values, flow rates in a number of subcortical areas being variable. Administration of trimethaphane or phentolamine did not affect ischemic and postischemic flow rates, nor did they alter recovery of EEG and sensory‐evoked responses, but trimetaphan blunted the changes in plasma concentrations of adrenaline and noradrenaline. Recovery experiments showed that 10 min of ischemia gave rise to clear signs of permanent brain damage, with a small number of animals developing postischemic seizures that led to the death of the animals in status epilepticus. After 15 min of ischemia, such alterations were more pronounced, and the majority of animals died. It is concluded that the short revival times noted are explained by the fact that the model induces near‐complete ischemia, and that recovery following forebrain ischemia is critically dependent on residual flow rates during the period of ischemia.
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| 7. |
- Wieloch, Tadeusz, et al.
(författare)
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Influence of Severe Hypoglycemia on Brain Extracellular Calcium and Potassium Activities, Energy, and Phospholipid Metabolism
- 1984
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Ingår i: Journal of Neurochemistry. - : Wiley. - 0022-3042 .- 1471-4159. ; 43:1, s. 160-168
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Tidskriftsartikel (refereegranskat)abstract
- Abstract: In the cerebral cortices of rats, during insulininduced hypoglycemia, changes in the concentrations of labile phosphate compounds [ATP, ADP, AMP, and phosphocreatine (PCr)] and glycolytic metabolites (lactate, pyruvate, and glucose) as well as phospholipids and free fatty acids (FFAs) were studied in relation to extracellular potassium and calcium activities. Changes in extracellular calcium and potassium activities occurred at approximately the onset of isoelectricity. The extracellular calcium activity dropped from 1.17 ± 0.14 mM to 0.18 ± 0.28 mM and the potassium activity rose from 3.4 ± 0.94 mM to 48 ± 12 mM (means ± SD). Minutes prior to this ionic change the levels of ATP, PCr, and phospholipids were unchanged while the levels of FFAs remained unchanged or slightly elevated. Following the first ionic change the steady‐state levels of ATP decreased by 40%, from 2.42 to 1.56 μmol/g. PCr levels decreased by 75%, from 4.58 to 1.26 μmol/g. Simultaneously, the levels of FFAs increased from 338 to 642 nmol/g, arachidonic acid displaying the largest relative increase, 33 to 130 nmol/g. The first ionic change was followed by a short period of normalization of ionic concentrations followed by a sustained ionic change. This was accompanied by a small additional decrease in ATP (to 1.26 μmol/g). The FEA levels increased to 704 nmol/g. There was a highly sig nificant negative correlation between the levels of FFAs and the energy charge of the tissue. The formation of FFAs was accompanied by a decrease in the phospholipid pool. The largest relative decrease was observed in the inositol phosphoglycerides, followed by serine and ethanolamine phosphoglycerides. After 10 min of isoelectricity the levels of phospholipids had decreased by 5.12 μmol/g while the levels of FFAs had increased by 0.46 μmol/g, indicating oxidative metabolism or washout of the released FFAs. The attenuation of the rapid initial changes in the levels of the energy metabolites and FFAs as well as the correlation between the energy charge and the levels of FFAs suggests that a new steady state is established following the first ionic change. The importance of these reactions for the development of hypogiycemic neuronal damage is discussed.
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