The effect of age on mitochondrial ultrastructure.

The ultrastructure of perfused livers and of mitochondrial fractions from 6-month-old and 30-month-old C57/BL mice were studied. In old mice the liver cell mitochondria were enlarged and rounded with a light 'foamy', vacuolated matrix, short cristae and a loss of dense granules. Quantitative studies showed a 60% increase in the mean size and an increased proportion of larger mitochondria in intact 30-month-old perfused livers. Endothelial and Kupffer cell mitochondria were smaller than those of the parenchymal cells. Mitochondria in pellets prepared from 6- and 30-month-old livers were rounded and condensed, although there were a few larger and 'foamy' mitochondria in the preparations from old mice. Up to 47% of large mitochondria in the old livers were lost during cell fractionation.     

The effect of praziquantel on Schistosoma mansoni.

3 x 10(-6)M praziquantel fails to completely paralyse miracidia and cercariae in a short time but they are not infective when maintained in the solution. 3 x 10(-5)M praziquantel prevents infected snails shedding cercariae but does not kill daughter sporocyts or developing cercariae. As the action of praziquantel on adult worms is not blocked by 10(-2)M mecamylamine, pempidine or carbachol, but is reduced by calcium depletion, it is suggested that praziquantel may act by permitting calcium influx to muscle cells causing them to contract.     

The effect of immigration on genetic control.

The effect of immigration of already inseminated females into the target area of a genetic control programme is analyzed. The sterile male technique and the use of cytoplasmically incompatible males are handled as special cases of the integrated genetical system proposed by Laven and Aslamakhan. For the sterile male technique explicit formulae are given for the critical immigration rate below which genetic control may be successful. If a strain is available which is advantageous to man, the integrated genetical system may be used to replace rather than to control the target population. An explicit formula is derived for the immigration level which can be sustained by a strain of a given fertility. In comparing the sterile male technique with the use of cytoplasmically incompatible males for control it is concluded that the former is to be chosen since the release rates of males necessary for population suppression would cause population replacement due to the unavoidable escape of even a very few females.     

The effect of counterions on melittin aggregation.

Melittin, a surface-active polypeptide from bee venom, has an overall hydrophobic N-terminus, with basic residues clustered at the C-terminus. In aqueous solution melittin exists as a mixture of monomer and tetramer, the monomer adopting a predominantly random-coil configuration, whereas the tetramer is rich in alpha-helix. The tendency of melittin to aggregate is dependent on the counter-anions present in solution, the effect being most marked with phosphate, decreasing in the order HPO4(2-) greater than SO4(2-) greater than ClO4- greater than Cl-.     

The effect of dexamethasone on urinary acidification.

Although it is well recognized that mineralocorticoids enhance renal acid excretion, the effect of glucocorticoids on renal acidification is unclear. Oral administration of dexamethasone to six healthy volunteers for 1 week at a daily dose of 4.5 mg was associated with mild respiratory alkalosis and a small but statistically significant increase in baseline urine pH. However, neither the ability to lower urine pH nor to excrete titratable acid and ammonium after NH4Cl acid-loading was altered. Administration of a single intravenous dose of dexamethasone sodium phosphate (7.5 mg) was associated with a significant rise in urine pH and potassium excretion and decreased titratable acid, ammonium , and phosphorus excretion in the absence of changes in blood acid-base status, creatinine clearance, or urine flow.     

The effect of fibrin structure on fibrinolysis.

Fibrin structure contributes to the regulation of the fibrinolytic rate. As the fibrin fiber size is decreased, the fibrinolytic rate also decreases. Fibrin structure was altered by either changing the ratio of thrombin to fibrinogen, i.e. altering the assembly rate or by adding a fibrin assembly inhibitor, iopamidol. Changes in the fibrinolytic rate were followed by measuring the time dependence of the decrease in the fiber mass/length ratio during fibrinolysis. A measure of the overall fibrinolytic rate was determined from the decrease in the mass/length ratio versus time. An 8-fold reduction in the fibrinolytic rate was seen on decreasing the mass/length ratio from 2.7 x 10(12) daltons/cm to 0.5 x 10(12) daltons/cm. It is shown that thin fibrin fibers have a decreased rate of conversion of plasminogen to plasmin by tissue plasminogen activator and that thin fibrin fibers are lysed more slowly than thick fibrin fibers.     

The effect of potassium chloride on the Bohr effect of human hemoglobin.

The normal and differential titration curves of liganded and unliganded hemoglobin were measured at various KCl concentrations (0.1 to 2.0 M). In this range of KCl concentrations, the curves for deoxyhemoglobin showed no salt-induced pK changes of titratable groups. In the same salt concentration range oxyhemoglobin showed a marked change in titration behavior which could only be accounted for by a salt-induced increase in pK of some titratable groups. These results show that the suppression of the alkaline Bohr effect by high concentrations of neutral univalent salt is not caused by a weakening of the salt bridges in deoxyhemoglobin but is due to an interaction of chloride ions with oxyhemoglobin. Measurements of the Bohr effect at various KCl concentrations showed that at low chloride ion concentration (5 times 10-3 M) the alkaline Bohr effect is smaller than at a concentration of 0.1 M. This observation indicates that at a chloride ion concentration of 0.1 M, part of the alkaline Bohr effect is due to an interaction of chloride ions with hemoglobin. Furthermore, at low concentrations of chloride ions the acid Bohr effect has almost vanished. This result suggests that part of the acid Bohr effect arises from an interaction of chloride ions with oxyhemoglobin. The dependence of the Bohr effect upon the chloride ion concentration can be explained by assuming specific binding of chloride ions to both oxy- and deoxyhemoglobin, with deoxyhemoglobin having the highest affinity.