Identification of T cell stimulatory epitopes from the 18 kDa protein of Mycobacterium leprae

We have used different mouse strains to examine in vivo andin vitro responses to the 18 kDa protein of Mycobacterium leprae,which appears to be strongly immunogenic in both mice and humans.B and T cell stimulatory epitopes recognised by different strainsof mice have been mapped using overlapping peptides that spanthe entire 18 kDa protein. Previous work established that Immunizationof mice with the 18 kDa protein results in specific antibodyproduction to common B cell epitopes and immunization of micewith peptides containing these B cell epitopes resulted in theinduction of specific IgG to only a limited subset of epitopesin each strain. Now we report that T cells purified from miceimmunized with peptides that stimulate antibody production,proliferate in vitro when rechallenged. The proliferating Tcells produce levels of IL-2 and IFN-, that indicate antigen-specificT helper type 1 cells are present in significant numbers. Thus,a comparison of in vivo and in vitro data suggests that T cellsbearing the phenotype associated with potentially protectivecell-mediated responses can be primed in vivo by epitopes onsmall peptides. Since T cells from both strains of mice arecapable of responding to the immunogenic synthetic peptidesin vitro, but give different responses to the same peptidesin vivo, factors other than epltope structure appear to influenceT cell subset activation. This may have important implicationsfor diseases such as leprosy where a polarized T cell responseappears to develop and for the development of synthetic subunitvaccines.     

Bcl-2 immunoreactive cells with immature neuronal phenotype exist in the nonepileptic adult human brain

Bcl-2, a cell death suppressor protein, is expressed during brain development but is largely down-regulated in the adult central nervous system. We previously reported strong expression of bcl-2 in small, "oligodendrocyte-like" cells (OLC) found in glioneuronal hamartias. These hamartias are microscopic cell rests found in temporal lobe resections from patients with intractable epilepsy and are considered a form of cerebral microdysgenesis. However, a causative relationship between these rests and seizures is not clear. We now report the identification, lineage characterization, and postnatal ontogeny of hamartia-like cell rests in temporal lobes of nonepileptic humans. Postmortem temporal lobes from 28 patients without history of neurologic disease (mean age = 53 years; range = 20 to 83 years) were studied. Microscopic cellular aggregates containing immature-appearing, bcl-2-immunoreactive cells (BIC) (identical to OLC) were observed in 23 of 28 (82%) temporal lobes from nonepileptic individuals. BIC were strongly immunoreactive for neuronal-specific class III beta tubulin, neuronal nuclear antigen, and MAP-2, but were consistently negative for neurofilament proteins and Ki67. Such cells were localized to subventricular regions of the caudal amygdala and often extended into the adjacent subcortical white matter and periamygdaloid cortex. BIC became less abundant with advancing age. These findings suggest that hamartia-like rests containing immature postmitotic neurons are normally present in the human brain and that glioneuronal hamartias may not always represent a maldevelopmental lesion associated with epilepsy.     

Aortic Stenosis and Patent Ductus Arteriosus: Pressure Gradients Pre- and Posttranscatheter Ductal Occlusion

Three patients with patent ductus arteriosus and moderate aortic stenosis had a marked reduction in aortic valve gradient following transcatheter ductal occlusion. The hemodynamic effects of an aortopulmonary shunt on the severity of left ventricular outflow obstruction and the implications on intervention are discussed.     

Angle grinder injuries: a cause of serious head and neck trauma

Over the past 12 months, the Victorian Trauma Centre at the Alfred Hospital, Melbourne, has dealt with serious head and neck injuries associated with angle grinder use. Three cases are presented, documenting the circumstances and severity of these injuries and subsequent management. Angle grinder injuries are a source of serious morbidity and mortality, much of which is preventable.     

Platelet size does not correlate with platelet age

The relationship between platelet size and in vivo aging was investigated in the baboon using size-dependent platelet subpopulations separated by counterflow centrifugation. The separation characteristics, size, lactate dehydrogenase (LDH) activity, and dense- body content of the baboon platelet subpopulations were similar to those previously observed in studies of human platelets. Three independent labeling techniques were used: (1) in vivo labeling with 75Se-methionine, (2) in vitro labeling with 51Cr, and (3) in vivo labeling with 14C-serotonin. Maximal incorporation of all three labels showed a close correlation between the mean platelet volume (MPV) of each fraction and the platelet radioactivity. The onset of incorporation and rate of accumulation of 75Se-methionine were comparable in all fractions when corrected for differences in volume, suggesting that platelet size heterogeneity was present from the time of release of the platelets from the bone marrow. Survival studies using 51Cr and 14C-serotonin showed no translocation of the label from one fraction to another in the circulation over time. In vivo survival values for the three radionuclides showed a slight but significant correlation between the lifespan and the MPV of the fractions. The data suggest that large platelets were not younger platelets, but rather platelets with a longer life-span. Platelet size heterogeneity is the result of production factors in the bone marrow and not maturation in the circulation.     

Zinc absorption in alcoholics using zinc-65

Alcoholism is occasionally complicated by zinc deficiency. We have assessed the possibility that malabsorption of zinc may be a potential cause. Using a dual isotope absorption technique the absorption of 65Zn in 18 alcoholic patients was 37% (13 +/- SD) and 56% (10 +/- SD) in a normal control group (p less than 0.001). The mean serum zinc in 55 alcoholic patients was 11.6 mumol/l (3.0 +/- SD) and in 36 normal volunteers the mean serum zinc was 13.6 mumol/l (1.8 +/- SD; p less than 0.001). This study suggests that chronic alcohol abuse will decrease the absorption of zinc and this may contribute towards the zinc deficiency occasionally associated with alcoholism.