Serological grouping of Treponema hyodysenteriae

Two Australian isolates of Treponema hyodysenteriae which did not fit within the current serological grouping system for these bacteria were examined by agarose gel double immunodiffusion tests (AGDP). Isolate Vic1 was serologically unique, and we propose that it becomes the type organism for a new sixth serological group of T. hyodysenteriae (Group F). Isolate Q1 was unusual in that lipopolysaccharide (LPS) extracted from it reacted strongly in AGDP with serum raised against the type organism for serogroup D (A1), and also weakly with serum raised against the type organism for serogroup B (WA1). The nature of this cross-reactivity was examined by using cross-absorbed antisera in AGDP, and by SDS-polyacrylamide gel electrophoresis (SDS-PAGE) and Western blot analysis. The pattern of serological cross-reactivity between Q1, A1 and WA1 was complex and was not fully defined, but the isolate Q1 apparently shared low molecular weight 'serogroup' LPS antigens with A1, and shared higher molecular weight LPS antigens with WA1. On this basis Q1 was designated as belonging to serogroup D, although it was recommended that this be qualified as D (B) to indicate the presence of weak cross-reactivity with serogroup B. Such serological cross-reactivity may have significance in relation to the development of immunity to T.hyodysenteriae. Isolate Q1 may be a potentially useful organism for vaccine development because of its ability to induce a good serological response to LPS of treponemes from both serogroups D and B.     

Potentiation of atherosclerotic lesions in rabbits by a high dietary level of vitamin E

1. Two experiments were conducted to determine whether or not high dietary levels of vitamin E affect the development of atherosclerotic lesions in aortas of cholesterol-fed (5 g/kg diet) rabbits that were mechanically deendothelialized by balloon catheterization. 2. In the first experiment, the aortas of rabbits fed 2000 mg vitamin E/kg diet (i.e. 50-fold their nutritional requirement) for 8 weeks showed no gross morphological differences, either within or outside experimentally damaged areas, from those of rabbits fed the nutritionally adequate control level (40 mg/kg) of the vitamin. 3. In the second experiment, rabbits fed 10,000 mg vitamin E/kg diet (i.e. 250-fold requirement) for 14-15 weeks showed significantly greater endothelial loss and plaque formation at aortic sites outside of the mechanically damaged area than did controls. Plasma cholesterol levels were very high (9000-14,000 mg/l) and were not affected by dietary vitamin E level until 10-12 weeks when they were reduced moderately (18%). 4. It is concluded that very high levels of vitamin E can potentiate spontaneous atherosclerotic lesions, and it is suggested that this effect may depend on high cholesterol status.     

Beta-amyloid activated microglia induce cell cycling and cell death in cultured cortical neurons

Immunocytochemical studies of postmortem human tissue have shown that the neurons at risk for degeneration in Alzheimer’s are marked by the ectopic expression of several cell cycle components. The current work investigates the roles that β-amyloid activated microglia might play in leading neurons to re-express cell cycle components. Stable cultures of E16.5 mouse cortical neurons were exposed to β-amyloid alone, microglial cells alone, or microglial cells activated by β-amyloid. Increased cell death was found in response to each of these treatments, however, only the amyloid activated microglial treatment increased the number of neurons that were positive for cell cycle markers such as PCNA or cyclin D and incorporation of BrdU. Double labeling with BrdU and TUNEL techniques verified that the ‘dividing’ neurons were dying, most likely through an apoptotic mechanism. The identity of the soluble factor(s) elaborated by the microglia remains unknown, but FGF2, a suspected neuronal mitogen, was ruled out. These results further support a model in which microglial activation by β-amyloid is a key event in the progression in Alzheimer’s disease.     

Modification of affect perception deficits in schizophrenia

This study investigated two strategies for improving facial affect perception in schizophrenia: monetary reinforcement and promoting facial feedback via mimicry of the expressions of target faces. A total of 40 inpatients with schizophrenia were administered the face emotion identification test during four phases: baseline, intervention, immediate post-test, and 1week follow-up. Subjects were randomly assigned to one of four interventions: repeated practice, monetary reinforcement, facial feedback, and a combination of reinforcement and facial feedback. Generalization of the intervention to a test of facial affect discrimination was also examined. The results showed that all groups of subjects, with the exception of those in the repeated practice group, improved in their ability to identify facial affect, with these effects showing some stability over time. There was limited evidence of these effects generalizing to the test of facial affect discrimination.