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Sedimentation equilibrium analysis demonstrated that preparations of bovine lipoprotein lipase contain a complex mixture of dimers and higher oligomers of enzyme protein. Enzyme activity profiles from sedimentation equilibrium as well as from gel filtration indicated that activity is associated almost exclusively with the dimer fraction. To explore if the enzyme could be dissociated into active monomers, 0.75 M guanidinium chloride was used. Sedimentation velocity measurements demonstrated that this treatment led to dissociation of the lipase protein into monomers. Concomitant with dissociation, there was an irreversible loss of catalytic activity and a moderate change in secondary structure as detected by circular dichroism. The rate of inactivation increased with decreasing concentrations of active lipase, but addition of inactive lipase protein did not slow down the inactivation. This indicates that reversible interactions between active species precede the irreversible loss of activity. The implication is that dissociation initially leads to a monomer form which is in reversible equilibrium with the active dimer, but which decays rapidly into an inactive form, and is therefore not detected as a stable component in the system.

It has been well established that elevated dietary tryptophan (TRP) levels can increase brain serotonin concentrations, thereby influencing serotonergic transmission. We previously examined interaction between dietary substrate (TRP: 0.15 and 0.6%) and the cofactor precursor (pyridoxine HCl: 3 and 3,000 mg/kg) on brain serotonin metabolism, observing significant increases in serotonin concentrations from such dietary interaction. The present experiments were designed to explore possible behavioral consequences of the substrate-cofactor interaction. After the IP injection of fenfluramine (FA: at 5, 10, 15, and 20 mg/kg), serotonin-mediated behavior traits and the appearance of flushing were observed in rats fed experimental diets as stated above. With a 5 mg/kg dose of FA, a differential dietary effect was most visible. However, at higher FA levels (15 and 20 mg/kg), such dietary effects were no longer discernible. The appearance of flushing was also dependent on dietary TRP intake and the dosage of FA. These results indicate a clear substrate-cofactor interaction on certain serotonin-mediated behavior traits in the rat.

We studied the metabolic effects of high dietary intakes of pyridoxine and of the substrate-cofactor interaction between dietary histidine or tryptophan and pyridoxine in rat brain. In the substrate-cofactor interaction study, histamine and serotonin levels were determined in rats fed elevated or requirement levels of substrate (histidine: 0.3% and 0.8%, tryptophan: 0.15% and 0.6%) and excess or requirement levels of pyridoxine HCl (7 mg vs. 3,000 mg/kg). Excess pyridoxine intake caused a differential effect on brain histamine concentration--inhibitory with the requirement level of histidine (-29%), and stimulatory (+21%) with the elevated level of histidine. When dietary tryptophan was fed at the requirement level, excess pyridoxine caused essentially no changes in hypothalamic serotonin and 5HIAA (-2%, -2%). With elevated tryptophan intake, excess pyridoxine significantly increased serotonin and 5HIAA (+32%, +20%) in the hypothalamus. These results indicate a clear interaction between substrate and coenzyme precursor which influences brain metabolism of histamine and serotonin.

This paper presents a three-dimensional Fourier descriptor (FD3) for shape representation/reconstruction. The FD3 is a double Fourier transform of serial cross-sectional contours of a shape in three dimensions (3D), which retains all shape information and gives a compact and invariant representation. The inverse Fourier transform of the FD3 reconstructs the original 3D shape; and it also estimates volume in the process. The upper bound of error introduced by the 3D reconstruction from the FD3 is derived in the sense of supremum norm. The FD3 method is compatible with medical imaging technologies such as computed tomography (CT) or magnetic resonance imaging (MRI). As an illustration of the FD3 methodology, a human head shape is reconstructed from its MR images.

Three-week-old male rats were fed for two weeks diets supplying inadequate, adequate, or excess amounts of histidine. After the 2-week feeding of the experimental diets, the rats were killed. Brain, gastrocnemius muscle, kidney and stomach were removed and analyzed for histamine and free-histidine as well as for the degradative enzyme, HMT, and the histamine-synthesizing enzyme HDC. The following results were obtained: As the levels of dietary histidine increased, (1) tissue concentrations of free-histidine and of histamine increased in all the tissues analyzed. (2) The increase of histamine was greatest in brain and stomach (5- and 4-fold, respectively), but less in kidney and muscle (2-fold). (3) HDC activity was not detected in muscle, but doubled from the lowest to the highest histidine intake in brain and increased almost 6-fold between the lowest and the highest histidine levels in stomach. (4) Kidney HDC decreased from the lowest to the two higher levels of dietary histidine. (5) HMT activity increased nominally in brain and not significantly in kidney; none was detected in either muscle or stomach. (6) Brain and kidney, tissues with considerable HMT activity, had almost no histamine. The increases in tissue histamine concentrations observed in the tissues analyzed generally reflected the changes and magnitudes of enzyme activities for HMT and HDC. The results in the rat differ in important ways from those previously observed in chickens as follows: (1) Histamine concentrations as a function in dietary histidine decreased in the chick. (2) Both HDC and HMT activities were present in chick muscle tissue. (3) HDC activity in chick stomach decreased sharply as a function of dietary histidine.