A model for institutional disturbances.
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CAMBRIDGE, U.K.--One of the few burgeoning areas of violence research here and in Europe is football hooliganism. With lower homicide rates than in the United States and fewer incidences of killing sprees such as the Littleton school shooting, Europeans are less concerned about violence than Americans are--and that translates into less money for research on the topic. Moreover, some scientists argue that strict regulation of animal studies has dealt a severe blow to a once-proud European tradition of behavioral research on animal aggression.
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The two enteropathogens Yersinia pseudotuberculosis and Yersinia enterocolitica penetrate eukaryotic cells in vitro through invasin, a surface-exposed protein. In contrast, Yersinia pestis, the causative agent of plague, is unable to enter mammalian cell lines, although the inv gene is present on its chromosome. Although 99.3% identical to the inv gene of Y. pseudotuberculosis, the Y. pestis inv gene was disrupted in its central region by a 708-bp IS200-like element. Multiple copies of this insertion sequence element were found within the genome of the plague bacillus.
A chromosomal locus (ure) involved in the production of urease activity in the bacterial pathogen Yersinia pseudotuberculosis was characterized. The genetic organization of the Y. pseudotuberculosis ure locus closely resembles that of the related ureolytic Yersinia species Y. enterocolitica. This locus encompasses seven open reading frames encoding polypeptides with predicted molecular weights of 10,894 (UreA), 15,820 (UreB), 61,001 (UreC), 25,801 (UreE), 24,551 (UreF), 20,330 (UreG), and 31,308 (UreD). The polypeptides have 85 to 96% identity with the corresponding Ure polypeptides of Y. enterocolitica serotype 0:8. Restriction fragment length polymorphisms of the ure loci from 12 unrelated Y. pseudotuberculosis strains produced by HaeIII and MboI indicate a low level of genetic variability of this locus in this species. The role of urease in the pathogenicity of Y. pseudotuberculosis was studied by constructing an isogenic urease-negative mutant obtained by disruption of structural gene ureB by aphA-3', which encodes kanamycin resistance. Experimental infection of mice with this mutant demonstrates that urease is not essential for Y. pseudotuberculosis virulence. Urease might be required mostly during the saprophytic life of this pathogen.
Yersinia-induced reactive arthritis is highly associated with HLA-B27, the role of which in defense against the triggering bacteria remains unclear. The aim of this study was to examine the capacity of rats transgenic for HLA-B27 to mount a cytotoxic T-lymphocyte (CTL) response against Y. pseudotuberculosis and to determine the influence of the HLA-B27 transgene on this response. Rats transgenic for HLA-B*2705 and human beta(2)-microglobulin of the 21-4L line, which do not spontaneously develop disease, and nontransgenic syngeneic Lewis (LEW) rats were infected with Y. pseudotuberculosis. Lymph node cells were restimulated in vitro, and the presence of for Y. pseudotuberculosis-specific CTLs against infected targets was determined. Infection of 21-4L rats triggered a CD8(+) T cell-mediated cytotoxic response specific for Y. pseudotuberculosis. Analysis of this response demonstrated restriction by an endogenous major histocompatibility complex molecule. However, no restriction by HLA-B27 was detected. In addition, kinetics studies revealed a weaker anti-Yersinia CTL response in 21-4L rats than in nontransgenic LEW rats, and the level of cytotoxicity against 21-4L lymphoblast targets sensitized with Y. pseudotuberculosis was lower than that against nontransgenic LEW targets. We conclude that HLA-B27 transgenic rats mount a CTL response against Y. pseudotuberculosis that is not restricted by HLA-B27. Yet, HLA-B27 exerts a negative effect on the level of this response, which could contribute to impaired defense against Yersinia.
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OBJECTIVES: The aim of this study is to describe the pattern of ill health after personal incapacitant spray (PIS) exposures reported to the National Poisons Information Service-London (NPIS-L) and the Chemical Incident Response Service and to evaluate the relation between sub-categories of PIS exposure and adverse health effects. METHODS: Case series study of patients reported to the NPIS-L, by attending medical personnel during the period 16 January to 31 September 1998. Data collected by questionnaire sent to these medical personnel. RESULTS: Several "adverse" symptoms, particularly dermatitis and blisters were reported for cases exposed to police PIS. These cases were more frequent than in those people exposed to non-police PIS. Adverse effects occurring more than six hours after exposure were also observed, which is in conflict with the recorded immediate, short lived, and self limiting symptoms that PIS are designed to cause. Most patients with persisting symptoms required further treatment. CONCLUSIONS: These findings suggest that the formulation of CS (o-chlorobenzylidine malononitrile) with MiBK (methyl iso-butyl ketone) used by the police is more harmful that has been previously assumed. If confirmed then the continued use of this formulation should be reviewed because of longer duration of adverse effects. Less concentrated formulations may reduce the severity or persistence of the adverse effects.
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