Long-term results of pectoralis major muscle transposition for infected sternotomy wounds.

During an 11.5-year period, 100 consecutive patients (79 male, 21 female) underwent repair of an infected sternotomy wound. Sixty-five patients had failed attempts at wound closure by other physicians. Median age was 61.5 years (range, 5 to 85 years). Reconstruction included muscle in 79 patients, omentum in 4, and both in 15. A total of 175 muscles were transposed, including 169 pectoralis major, 3 rectus abdominis, 2 external oblique, and 1 latissimus dorsi. Median number of operations was four (range, 1 to 11). Mechanical ventilation was required in 30 patients. Two perioperative deaths occurred, one related to sepsis. Median follow-up was 4.2 years (range, 1.3 to 13.5 years). Twenty-six patients had recurrent infection. Median time from our closure to recurrence was 5.5 months (range, 0.3 to 27.6 months). Cause of recurrence was inadequate removal of cartilage in 16 patients, bone in 6, and retained foreign body in 4. Eighteen patients had the wound reopened with further resection; 10 had another muscle or omentum transposition. There were 30 late deaths, only one related to recurrent infection. At the time of death or last follow-up, 92 patients had a healed chest wall. Transposition of the pectoralis major muscle remains an excellent method of management for infected sternotomy wounds. Failure is directly related to persistent infection of cartilage, bone, or retained foreign bodies.     

Cloning and characterization of Ca(2+)-dependent and Ca(2+)-independent PKCs expressed in Aplysia sensory cells

We isolated cDNA clones from an Aplysia sensory-cell library encoding two isoforms of protein kinase C (PKC). Several isozyme-specific regions are conserved in the Aplysia kinases, notably the variable regions V5 in the Ca(2+)-dependent PKC (Apl I) and V1 in the Ca(2+)-independent PKC (Apl II). Neuronal proteins with the properties expected of these two isoforms can be identified with antibodies raised against peptides synthesized from the amino acid sequences deduced from the clones. Sacktor and Schwartz (1990) measured the proportion of kinase activity that can be translocated to membrane in Aplysia sensory neurons and ganglia by stimuli that produce the presynaptic facilitation underlying behavioral sensitization. Much less Apl I and Apl II are translocated, suggesting that still other isoforms of PKC exist in these cells.     

Neuropeptide levels in the basal ganglia of aged common marmosets following prolonged treatment with MPTP

Summary Aged common marmosets were treated with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP; 0.5–2.0 mg/kg/week i.p.) for 16 or 24 weeks, observed for a total of 30 weeks and then killed for measurement of biochemical pramaters in basal ganglia. The MPTP treatment induced a marked depletion in dopamine, 3,4-dihydroxyphenylacetic acid and homovanillic acid levels in the caudate nucleus and putamen. In contrast, the concentrations of five neuropeptides: [Met⁵]-enkephalin, [Leu⁵]-enkephalin, cholecystokinin, substance P and neurotensin as measured by a combined HPLC/RIA method, remained unaltered in all basal ganglia regions examined. Enkephalin precursor levels, as reflected by cryptic [Met⁵]-enkephalin content, were increased in the putamen, but not in the caudate nucleus, as a consequence of MPTP administration. Cryptic [Leu⁵]-enkephalin content remained unchanged in the striatum of MPTP treated marmosets. Overall, these results suggest an increase in striatal [Met⁵]-enkephalin release following chronic MPTP treatment of aged marmosets. However, the chronic treatment of aged marmosets with MPTP does not reproduce the neuropeptide alterations characteristic of Parkinson's disease.     

Ticlopidine and clopidogrel (SR 25990C) selectively neutralize ADP inhibition of PGE1-activated platelet adenylate cyclase in rats and rabbits

Ticlopidine and its potent analogue, clopidogrel, are powerful inhibitors of ADP-induced platelet aggregation. In order to improve the understanding of this ADP-selectivity, we studied the effect of these compounds on PGE1-stimulated adenylate cyclase and on the inhibition of this enzyme by ADP, epinephrine and thrombin. Neither drug changed the basal cAMP levels nor the kinetics of cAMP accumulation upon PGE1-stimulation in rat or rabbit platelets, which excludes any direct effect on adenylate cyclase or on cyclic nucleotide phosphodiesterase. However, the drop in cAMP levels observed after addition of ADP to PGE1-stimulated control platelets was inhibited in platelets from treated animals. In contrast, the drop in cAMP levels produced by epinephrine was not prevented by either drug in rabbit platelets. In rat platelets, thrombin inhibited the PGE1-induced cAMP elevation but this effects seems to be entirely mediated by the released ADP. Under these conditions, it was not surprising to find that clopidogrel also potently inhibited that effect of thrombin on platelet adenylate cyclase. In conclusion, ticlopidine and clopidogrel selectively neutralize the ADP inhibition of PGE1-activated platelet adenylate cyclase in rats and rabbits.     

Sex effects in defensive behavior: Baseline differences and drug interactions

Female rats consistently show a pattern of differences in defensive behaviors compared to males which parallel the effects of exposure to a nonpainful threat stimulus (cat or cat odor) in the same tests and measures. These indications of greater defensiveness for females are particularly common in situations involving potential, as opposed to actual and present, threat, a factor which probably also reflects ceiling or floor effects in situations involving very intense defensiveness. In addition, pharmacological studies indicate sex differences in the effects of selective serotonin (5-HT) receptor agonists and antagonists on defensive responding. These findings indicate that sex effects must be considered in studies of the pharmacological control of defensive behaviors, and suggest that responsivity to sex effects may be an additional criterion for the suitability of animal models of anxiety.     

Induction of immunoreactive proliferating cell nuclear antigen (PCNA) in goldfish retina following intravitreal injection with tunicamycin.

Effects of a photoreceptor-specific biotoxin, tunicamycin (TM), injected intravitreally into the goldfish eye at one side, were explored on electroretinograms (ERGs) and proliferating cell nuclear antigen-immunoreactive (PCNA-ir) nuclei, representing the mitotic activity of rod precursors, in the retina at both sides. The eye-cup preparations were made for ERG recording, and the retinas were isolated and processed as cryosections or wholemounts by a routine immunohistochemical method for visinin (cones), opsin (rods), tyrosine hydroxylase (dopaminergic cells) and proliferating cell nuclear antigen (PCNA), at various intervals after intravitreal injection with TM (1.0 micrograms/eye). On some thin sections, autoradiographic study was combined following intravitreal injection with [3H]thymidine (TdR, 0.1 microCi/eye). The dose of TM used heavily destroyed cones and rods only in the treated retinas 2-15 days after injection, the photoreceptors being renewed for further 15-20 days. Approximately in parallel, ERGs were largely impaired 2-10 days after TM injection and recovered for 10-20 days. However, intravitreal TM altered the distribution and density of PCNA-ir nuclei in both treated and untreated retinas. The density of PCNA-ir nuclei reduced at first (on days 1 and 2), and then clustered and rapidly increased on days 3-5 and maintained at high levels with diffuse distribution over the whole area, particularly in the treated retinas, up to 60 days after TM injection; the maximum peak of 3.7 and 20 times the initial level was seen on day 20 in the outer nuclear layer (ONL) and inner nuclear layer (INL), respectively. PCNA-ir nuclei were found to be abundant in the ONL even after the photoreceptors and ERGs had been restored in the treated retinas on day 20, suggesting a kind of overproduction of retinal cells. The autoradiographic study provided comparable results to those obtained with PCNA immunohistochemistry. The mechanism by which damage to the treated retina causes rod precursor cells to proliferate in the untreated retina remains unresolved.     

Is interleukin 2 a neuromodulator in the brain?

A bidirectional flow of information exists between the CNS and the neuroendocrine and immune systems, representing an important homeostatic mechanism in the body. Lymphokines and other products of immunocompetent cells seem to play a crucial role in this communication and seem to exert powerful effects on neurones in the brain. In this article, Giuseppe Nisticò and Giovambattista De Sarro describe the central effects following interleukin 2 (IL-2) microinfusion into several areas of the rat brain. The locus coeruleus seems to be the main site in the brain through which IL-2 exerts soporific effects. In addition, the possible transducing mechanisms coupling IL-2 receptor stimulation and the electroencephalogram (EEG) spectrum power responses elicited from the locus coeruleus seem to involve stimulation of specific receptors coupled to adenylate cyclase through a Gi protein.     

Curriculum for musculoskeletal radiology.

Although general suggestions have been made regarding a radiology residency curriculum, no specific list of entities has been offered. Over the past ten years, we have developed a resident-run morning conference in musculoskeletal radiology that is supervised by faculty and covers a specific curriculum. We offer our curriculum as an example that may assist other departments in developing their own curricula.