Pulmonary metabolism of epoxides.

Activities of epoxide hydrase (EH) and glutathione S-transferase (GST) have been measured in pulmonary tissue from several species. On the basis of total organ activity, pulmonary tissue has less capacity than liver tissue to metabolize epoxides. Pulmonary EH and GST appear to be refractory to induction by typical agents. Rat pulmonary GST will conjugate a variety of epoxides, but K-region epoxides are metabolized at lower rates than alkene oxides. In the isolated perfused rabbit lung, benzo (a) pyrene-4,5-oxide (BPO) is metabolized by EH and GST at similar initial rates, but EH activity is lost after a few minutes, apparently owing to inadequate local substrate levels. GST from rabbit lung cytosol has been separated by chromatographic methods into six peaks of enzymic activity (toward 1-chloro-2,4-denitrobenzene). Of these peaks, all six metabolized BPO and two metabolized styrene oxide. Although EH and GST are less active in lung than in liver, pulmonary metabolism of epoxides is important because this tissue must be able to protect itself from arene oxides generated by pulmonary oxidative metabolism of polycyclic aromatic hydrocarbons.     

Studies of insulin release and rat pancreatic islet metabolism with diastereomers of D-glucose

Studies of insulin release with diastereomers and other analogues of D-glucose demonstrated that only sugars which undergo oxidation to CO₂ stimulate insulin release by the pancreatic islet. None of the non-metabolizable diastereomers of glucose stimulated insulin release in the presence of a substimulatory concentration of glucose for fuel. Although 5.5 mM glucose formed 77% as much CO₂ as 16.7 mM mannose and twice that of 16.7 mM fructose, 5.5 mM glucose did not stimulate insulin release whereas 16.7 mM mannose and fructose did stimulate insulin release. These results indicate that the important stimulus for glucose-induced insulin release involves metabolism of glucose, but that the stimulus does not involve solely a fuel function of glucose.     

Pathogenesis of the "sentinel headache" preceding berry aneurysm rupture.

Pathologic examination in a case of fatal intracerebral hemorrhage from a berry aneurysm showed that the "sentinel" or warning headache in this patient was due to the leakage of blood into the subarachnoid space through a previous small tear in the wall of her saccular aneurysm. Oribital pain, transient, dysphasia, dizziness and, later, meningismus might have prompted the performing of a lumbar puncture to determine the presence of blood in the cerebrospinal fluid. This type of event is the likely pathogenetic mechanism for the premonitory headache that may precede a lethal rupture of a saccular aneurysm.     

Dynamic population epidemic models.

Most multipopulation epidemic models are of the contact distribution type, in which the locations of successive contacts are chosen independently from appropriate contact distributions. This paper is concerned with an alternative class of models, termed dynamic population epidemic models, in which infectives move among the populations and can infect only within their current population. Both the stochastic and deterministic versions of such models are considered. Their threshold behavior is analyzed in some depth, as are their final outcomes. Velocities of spread of infection are considered when the populations have a spatial structure. A criterion for finding the equivalent contact distribution epidemic for any given dynamic population epidemic is provided, enabling comparisons to be made for the velocities and final outcomes displayed by the two classes of models. The relationship between deterministic and stochastic epidemic models is also discussed briefly.     

Nicotinic Receptor-Mediated Release of Noradrenaline in the Human Neuroblastoma SH-SY5Y

Abstract: Dimethylphenylpiperazinium iodide (a nicotinic agonist) evokes noradrenaline release from human neuroblastoma SH-SY5Y cells that have been pretreated with 12- O -tetradecanoylphorbol 13-acetate for 8 min. This effect of dimethylphenylpiperazinium iodide was inhibited by 1 μ M mecamylamine but not by 1 μ M atropine, which suggests that SH-SY5Y cells express nicotinic receptors coupled to the release of noradrenaline. Dimethylphenylpiperazinium iodide-evoked release was enhanced by 5 μ M Bay K 8644 (an L-type calcium agonist) and inhibited by 1 μ M nifedipine. Dimethylphenylpiperazinium iodide depolarised SH-SY5Y cells and enhanced the level of intracellular calcium in cells loaded with fura 2. The effects of dimethylphenylpiperazinium iodide on noradrenaline release, depolarisation, and intracellular calcium levels were all inhibited by 1 μ M desmethylimipramine. The results of this study show that nicotinic receptors in SH-SY5Y cells stimulate noradrenaline release by activation of L-type calcium channels.