Most cases of severe Staphylococcus aureus disease cannot be explained by the action of a single virulence determinant, and it is likely that a number of factors act in combination during the infective process. This study examined the relationship between disease in humans and a large number of putative virulence determinants, both individually and in combination. S. aureus isolates (n ‫؍‬ 334) from healthy blood donors and from patients with invasive disease were compared for variation in the presence of 33 putative virulence determinants. After adjusting for the effect of clonality, seven determinants (fnbA, cna, sdrE, sej, eta, hlg, and ica) were significantly more common in invasive isolates. All seven factors contributed independently to virulence. No single factor predominated as the major predictor of virulence, their effects appearing to be cumulative. No combinations of the seven genes were either more or less likely to cause disease than others with the same number of virulence-associated genes. There was evidence of considerable horizontal transfer of genes on a background of clonality. Our findings also suggested that allelic variants of a polymorphic locus can make different contributions to the disease process, further study of which is likely to expand our understanding of staphylococcal disease pathogenesis.

Purpose To investigate, visualize and quantify the physiology of the human placenta in several dimensions ‐ functional, temporal over gestation, and spatial over the whole organ. Methods Bespoke MRI techniques, combining a rich diffusion protocol, anatomical data and T2* mapping together with a multi‐modal pipeline including motion correction and extracted quantitative features were developed and employed on pregnant women between 22 and 38 weeks gestational age including two pregnancies diagnosed with pre‐eclampsia. Results A multi‐faceted assessment was demonstrated showing trends of increasing lacunarity, and decreasing T2* and diffusivity over gestation. Conclusions The obtained multi‐modal acquisition and quantification shows promising opportunities for studying evolution, adaptation and compensation processes.

Endometriosis is a common women's health problem that is characterized by the presence of tissue resembling endometrium outside the uterus. The condition causes painful periods, chronic pelvic pain, and subfertility, which are potentially debilitating; and it affects millions of women worldwide. The diagnosis is made on visual inspection of the pelvis, usually at laparoscopy. The natural history is unknown, and well-controlled experiments are difficult to perform because of the need for repeated surgical procedures to assess endometriotic lesions over time. Thus, despite over 50 years' research, the cause of endometriosis remains unclear, and treatment options are limited. Animal models provide an invaluable tool to study risk factors, prevalence, and the natural history of endometriosis especially in those menstruating nonhuman primates that develop the disease spontaneously. Many of the practical problems associated with studying the disease in humans can therefore be overcome. The pathophysiology of endometriosis can also be investigated and new treatments assessed in both nonprimates and nonhuman primates, with "disease" induced by placing autologous uterine tissue in ectopic sites, or human endometrium in the case of nude mice. However, although nonprimates have obvious advantages as a model, the extent to which the induced lesions are truly representative of the disease itself is debatable. This review explores the value of the experimental models that have been used to date.

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