A complication of peribulbar block in a patient with exophthalmos

A patient with marked exophthalmos secondary to thyroid eye disease presented for tarsorrhaphy and removal of orbital fat. A single superolateral peribulbar injection was performed. After injection of 3.5 ml of local anaesthetic solution, the globe suddenly dislocated anteriorly. This complication has not been described previously. In patients with exophthalmos, general anaesthesia should be considered as the method of choice for ophthalmic procedures.      

Maintenance of targeting errors by isthmo-optic axons following the intraocular injection of tetrodotoxin in chick embryos.

We have studied the role of electrical activity in the elimination of axonal targeting errors, which is a normal process in brain development. The experiments were focused on the isthmo-optic nucleus (ION), which, in adults, projects in topographical order on the contralateral retina. During embryogenesis, however, a few isthmo-optic neurons project to the ipsilateral retina, and many project to topographically inappropriate parts of the contralateral one; both kinds of targeting error are known to be eliminated by the deaths of the parent neurons. We injected tetrodotoxin (TTX) intraocularly at embryonic days 13 and 15 and, on the latter, applied a retrograde label to the retina of the same eye. Embryos were fixed at embryonic day 17. In some embryos, the label was a peripherally placed fleck of the carbocyanine dye "diI"; the resulting retrogradely labeled neurons in the contralateral ION were much more widely scattered in the TTX-injected embryos than in controls (errors in topography). In other embryos, the label was a solution of rhodamine-B-isothiocyanate (RITC) injected into the vitreous body; this yielded several ipsilaterally labeled isthmo-optic neurons in the TTX-injected embryos, but virtually none in the controls. The numbers of both kinds of aberrantly projecting neuron approached those previously reported near the beginning of the ION's period of neuronal death. We conclude that electrical activity plays an important role in the elimination of axonal targeting errors in the chick embryo's isthmo-optic system.     

Mitochondrial genome: defects, disease, and evolution.

Defects of mitochondrial function are often caused by defects of the mitochondrial genome. The hypothesis that defective organelles may spread through syncytial tissues as a result of a process of subcellular Darwinian selection is proposed. Tissues are likely to be involved in mitochondrial disease if they are syncytial, are derived from a few embryonic cells only, have little redundancy of function, and are subject to repeated metabolic stress. These effects, together with the random distribution of genetically heterogeneous mitochondria within the fertilised zygote, may account for the varied clinical pictures of mitochondrial disease. Evolution will have favoured the shift of mitochondrial DNA sequences to the nucleus, once the differentiation of tissues had created body compartments in which defective mitochondria could flourish to the detriment of the organism. This model of mitochondrial disease allows the generation of several predictions, testable using currently available laboratory techniques. Avenues of potential therapeutic value are indicated, including the avoidance of hypoglycaemia and the use of selective mitochondrial toxins.     

Benzylamine oxidase in normal and atherosclerotic human aortae

Assays of serum benzylamine oxidase (BzAO) have led some workers to postulate a relationship between elevated BzAO activity and diseases characterized by proliferating connective tissue. The present study was designed to determine whether BzAO activity of a cellular tissue is also affected. BzAO was assayed in homogenates of normal and atherosclerotic human aortae. Characterization done in normal aortae showed that BzAO is not a classical monoamine, diamine, polyamine, or lysyl oxidase, nor is it a ceruloplasmin. The enzyme is heat stable at 60 degrees C and is associated primarily with the microsomal fraction on density centrifugation. Compared with phenylethylamines and indoleamines, benzylamine is the best substrate. BzAO is sensitive to inhibition by hydrazines and chymotrypsin but not trypsin, and is insensitive to Triton X-100 and sulfhydryl-group blockade. BzAO activity of atherosclerotic plaque (expressed per gram wet weight or per milligram protein) was decreased markedly compared to that in adjacent, nonplaque regions and in normal aortae. However, on a per milligram DNA basis, the BzAO activity of plaque did not differ from that of nonplaque tissue. We conclude that there is a decreased cell population density in plaque, a contention supported by kinetic analysis. Plaque BzAO showed a decreased Vmax with no change in the Km of benzylamine compared with nonplaque tissue. Thus, if a relationship exists between BzAO activity and proliferating connective tissue, it is not apparent at the level of the cellular enzyme in atherosclerotic aortae of man.