Tyrosine hydroxylase expression within Balb/C and C57Black/6 mouse locus coeruleus. I. Topological organization and phenotypic plasticity of the enzyme-containing cell population

Tyrosine hydroxylase phenotype expression was investigated in the catecholaminergic population of the locus coeruleus neurons of two pure inbred mouse strains, Balb/C and C57Black/6. Therefore, we have characterized the precise organization of tyrosine hydroxylase-expressing perikarya population, in control animals and following RU24722 treatment, which is known to induce tyrosine hydroxylase expression. Serial coronal sections were selected along the caudo-rostral extent of the structure and were processed for tyrosine hydroxylase immunocytochemistry. Three days after the treatment, an increase in the number of cells which expressed tyrosine hydroxylase was observed all along the locus coeruleus in the Balb/C strain only. This increase equalized the catecholaminergic neuron populations of the two strains. In the caudal subdivision of the structure, these newly detected perikarya were intermingled with the perikarya which expressed tyrosine hydroxylase in control conditions. In the rostral half, the additional immnunoreactive perikarya enlarged the mean coerulean space, defined as the area delimited by the tyrosine hydroxylase-containing perikarya. These results demonstrate a plasticity of the tyrosine hydroxylase phenotype expression, topologically organized and specific to the Balb/C strain.     

Up-regulation of the iC3b receptor (CR3) is neither necessary nor sufficient to promote neutrophil aggregation

The iC3b receptor (CR3) is required for neutrophil adhesive functions, including homotypic aggregation. Because stimuli that enhance neutrophil adhesion also induce up-regulation of surface CR3, it is widely held that these two responses are causally related. We have dissociated CR3 display (immunofluorescence) from CR3 function (aggregation). Neutrophils isolated at 4 degrees C and rewarmed to 37 degrees C up-regulated surface CR3 twofold, but did not aggregate. The kinetics of FMLP-induced CR3 up-regulation were discordant with those of aggregation. In the absence of extracellular divalent cations, CR3 expression increased twofold after exposure to FMLP, but neutrophils did not aggregate. FMLP elicited 3.5-fold more aggregation than the ionophore A23187, yet less than one-half as much CR3 up-regulation. 3 mM sodium salicylate inhibited aggregation 55 +/- 4%, but had no effect on CR3 up-regulation. Conversely, 1 mM tetracaine completely inhibited CR3 up-regulation, while significantly enhancing aggregation. Neutroplasts expressed CR3, but did not up-regulate the receptor; in contrast, FMLP induced CR3-dependent aggregation of neutroplasts. We conclude that, although constitutive surface CR3 is required for neutrophil aggregation, the up-regulation of CR3 is neither necessary nor sufficient to promote cell-cell adhesion.     

Myocardial visualization on a perfusion lung scan

Myocardial activity was noted on a lung scan performed following the i.v. administration of Tc-99m macroaggregated albumin. The patient had primary pulmonary hypertension with a right-to-left shunt through a functionally patent foramen ovale.     

Increased levels of cyclic adenosine-3',5'-monophosphate in human polymorphonuclear leukocytes after surface stimulation.

Levels of cyclic AMP (cAMP) (but not cyclic GMP) in suspensions of human polymorphonuclear leukocytes (PMN) increased promptly after exposure of the cells to stimuli such as the chemotactic peptide N-formyl methionyl leucyl phenylalanine, the immune complex bovine serum albumin/anti-bovine serum albumin and calcium ionophore A23187. cAMP increased rapidly, reaching a maximum of twice the basal level 10--45 s after stimulation; after 2--5 min the amount of cAMP had subsided to basal levels. Elevations in cAMP levels were concurrent with, or followed, membrane hyperpolarization (measured by uptake of the lipophilic cation triphenylmethyl phosphonium) and always preceded lysosomal enzyme release and superoxide anion (O2) production. Elevated cAMP levels could be uncoupled from these later events by removal of extracellular divalent cations, replacement of extracellular Na+ with K+ or choline+, and by use of low concentrations of stimulus; each of these conditions virtually abolished lysosomal enzyme release and O2 generation, while leaving the stimulated elevation of cAMP levels unimpaired. Calcium ionophore A23187 did not provoke membrane hyperpolarization, thus uncoupling changes in membrane potential from changes in cAMP levels. These data suggested that cAMP is not a critical component in the earliest steps of stimulus-secretion coupling. Surface stimulation of cells pretreated with prostaglandins E1 or I2 yielded very high levels of cAMP; these high levels may be an important part of the mechanism by which stable prostaglandins inhibit lysosomal enzyme release and O2 generation.     

The radionuclide detection of lower gastrointestinal bleeding sites

A retrospective review of two years' experience with radionuclide screening to detect lower gastrointestinal bleeding sites was conducted at New York's Montefiore Medical Center. Of 82 studies performed in 63 patients, 13 identified active bleeding sites. Only three of eight angiograms obtained in these 13 patients were positive. Thirteen contrast angiograms were performed in the group of 50 patients with negative radionuclide studies of which ten were negative and one was equivocal. The results of this study suggest that the Tc-99m sulfur colloid study for active lower gastrointestinal (GI) bleeding is an effective screening procedure. Positive studies help determine which vessel to catheterize selectively if an angiogram is to be performed. If vascular ectasis is still suspected following a negative radionuclide study, contrast angiography can be more efficaciously performed on a nonemergent basis.