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Biomechanical analyses are commonly conducted to investigate how craniofacial form relates to function, particularly in relation to dietary adaptations. However, in the absence of corresponding muscle activation patterns, incomplete muscle data recorded experimentally for different individuals during different feeding tasks are frequently substituted. This study uses finite element analysis (FEA) to examine the sensitivity of the mechanical response of a Macaca fascicularis cranium to varying muscle activation patterns predicted via multibody dynamic analysis. Relative to the effects of varying bite location, the consequences of simulated variations in muscle activation patterns and of the inclusion/exclusion of whole muscle groups were investigated. The resulting cranial deformations were compared using two approaches; strain maps and geometric morphometric analyses. The results indicate that, with bite force magnitude controlled, the variations among the mechanical responses of the cranium to bite location far outweigh those observed as a consequence of varying muscle activations. However, zygomatic deformation was an exception, with the activation levels of superficial masseter being most influential in this regard. The anterior portion of temporalis deforms the cranial vault, but the remaining muscles have less profound effects. This study for the first time systematically quantifies the sensitivity of an FEA model of a primate skull to widely varying masticatory muscle activations and finds that, with the exception of the zygomatic arch, reasonable variants of muscle loading for a second molar bite have considerably less effect on cranial deformation and the resulting strain map than does varying molar bite point. The implication is that FEA models of biting crania will generally produce acceptable estimates of deformation under load as long as muscle activations and forces are reasonably approximated. In any one FEA study, the biological significance of the error in applied muscle forces is best judged against the magnitude of the effect that is being investigated.

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OBJECTIVES: To evaluate the use of intravenous ketamine for procedural sedation in adults attending the emergency department. METHODS: A prospective study was performed over a 2-year period in 92 patients who received intravenous ketamine for procedural sedation in the emergency department of St Thomas' Hospital. All patients received 0.5-1.0 mg/kg ketamine intravenously for the procedure. Pulse rate, blood pressure oxygen saturations and incidence of adverse events (clonic movements, hypersalivation, laryngospasm, recovery agitation and vomiting) were recorded for all patients. RESULTS: Adequate sedation was obtained in 91 of the 92 patients (98.9%) and successful completion of the procedure was achieved in 91 patients (98.9%). Adverse events occurred in 20 patients (21.7%). Four patients (7%) developed clonic movements, none of which required treatment. Twelve patients (13.0%) developed recovery agitation. In five cases the agitation was transient and required no treatment; the other seven patients were treated with intravenous midazolam. One of the patients who experienced recovery agitation also developed vomiting. Two other patients vomited, and one patient had vomiting and hypersalivation. One further patient developed hypersalivation. There were no reported episodes of laryngospasm. CONCLUSIONS: Ketamine is an effective agent for procedural sedation in the emergency department. There were no serious adverse events associated with its use, but there is a significant incidence of recovery agitation which may require treatment with a benzodiazepine.

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Detecting some of the genes that influence disease resistance would improve our understanding of the processes that cause disease and also simplify disease control. Genes within the major histocompatibility complex (mhc) are strong candidates for disease resistance and they have been intensely studied for the last 30 years. Recently, several groups working independently have reported the existence of alleles within the mhc that are associated with enhanced resistance to nematode infection. This article uses hindsight to describe some of the potential pitfalls that hinder the search for valid disease resistance genes. The search requires a good understanding of disease biology, molecular genetics, statistical genetics and especially, the design and analysis of experiments. The power to detect mhc effects is quite low and is quite sensitive to the frequency of the putative resistance alleles.

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Acute graft-versus-host disease (GvHD) is an inflammatory disorder associated with generalised damage to epithelial tissues, including the gastrointestinal tract. There is increasing evidence that this pathology is due to the effects of cytokines on epithelial cell proliferation and differentiation. However, it is unclear whether factors derived from immune cells act directly on epithelial cells or via other mediators whose principal role is to regulate cell growth under normal or diseased conditions. We show here that the increased crypt cell turnover and lymphocytic infiltration which occurs in the jejunum of mice with graft-versus-host reaction (GvHR) is accompanied by decreased enterocyte expression of transforming growth factor beta 2. Administration of exogenous TGF beta inhibits the crypt hyperplasia of GvHR and reduces systemic manifestations of GvHR such as increased splenic natural killer (NK) cell activity. In parallel, neutralisation of endogenous TGF beta by monoclonal antibody exacerbates both the proliferative and inflammatory components of intestinal and systemic GvHR. Thus, the immune system may induce epithelial pathology at least in part by altering the production of endogenous TGF beta. This cytokine may therefore prove a useful focus for therapeutic intervention in immunopathologies such as GvHD.

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Soil erosion is a major environmental threat to the sustainability and productive capacity of agriculture. During the last 40 years, nearly one-third of the world's arable land has been lost by erosion and continues to be lost at a rate of more than 10 million hectares per year. With the addition of a quarter of a million people each day, the world population's food demand is increasing at a time when per capita food productivity is beginning to decline.

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Nine enzyme activity variants and one charge variant of liver/erythrocyte pyruvate kinase have been found amongst laboratory and wild mice. Four of the enzyme activity variants were previously reported to be caused by allelic differences in the structural gene, Pk-1s. Analysis of two putative regulatory gene mutations is now reported, both of which map at, or close to, the structural gene on chromosome 3. One of these mutations, in the inbred strain SWR, is tissue specific, affecting enzyme concentration in the liver but not the erythrocyte the other, which arose in a mutation experiment, doubles the enzyme concentration in both tissues. The organization and the nomenclature in the [Pk-1] gene complex are discussed and are compared with the organization of other comprehensively analysed gene complexes in the mouse.

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Nine enzyme activity variants of liver/erythrocyte pyruvate kinase have been found amongst laboratory and wild mice. Four of these variants have been shown by biochemical and immunological criteria to be mutations of the structural gene, Pk-1s. These four structural gene mutations, and two regulatory gene mutations, define the gene complex, [Pk-1]. One allele of the structural gene, Pk-1sl, found in the inbred strain C57BL, has an unusual phenotype and affects the expression of pyruvate kinase in the liver but not erythrocyte. A possible mechanism for this tissue-specific structural gene mutation is suggested.

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Complexing iodine with povidone (polyvinylpyrrolidone) or surfactants significantly limits the quantity of free iodine. Reduction of the free iodine level eliminates the adverse properties of staining, instability, and irritation and also alters bactericidal activity. Addition of detergents to create surgical scrub solutions further reduces the activity of iodine. In vitro testing indicated that the bactericidal activity of iodophors was inferior to that of uncomplexed aqueous iodine. In vivo tests proved that aqueous iodine significantly potentiated the development of infection. Although the povidone iodophor did not enhance the rate of wound or infection, it offered no therapeutic benefit when compared with control wounds treated with saline solution. Addition of detergents to the povidone iodophor was deleterious, with the wounds exposed to this combination displaying significantly higher infection rates than untreated control wounds. Based on these results, aqueous iodine solutions and iodophor surgical scrub solutions should not be used on broken skin. Aqueous iodophors can be used in wounds, but no therapeutic benefit from such use was found in this study.

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