Mister Mary Somerville: Husband and Secretary

Mary Somerville’s life as a mathematician and savant in nineteenth-century Great Britain was heavily influenced by her gender; as a woman, her access to the ideas and resources developed and circulated in universities and scientific societies was highly restricted. However, her engagement with learned institutions was by no means nonexistent, and although she was 90 before being elected a full member of any society (Società Geografica Italiana, 1870), Somerville (Figure 1) nevertheless benefited from the resources and social networks cultivated by such institutions from as early as 1812. A key intermediary between Somerville and these societies was her husband, Dr. William Somerville, whose mediation was vital to her access to knowledge and her subsequent career as a scientific author. In this paper we will consider how spousal cooperation enabled the overcoming of gendered barriers to scientific institutions in the nineteenth century

Why Functional Pre-Erythrocytic and Bloodstage Malaria Vaccines Fail: A Meta-Analysis of Fully Protective Immunizations and Novel Immunological Model

Background: Clinically protective malaria vaccines consistently fail to protect adults and children in endemic settings, and at best only partially protect infants. Methodology/Principal Findings: We identify and evaluate 1916 immunization studies between 1965-February 2010, and exclude partially or nonprotective results to find 177 completely protective immunization experiments. Detailed reexamination reveals an unexpectedly mundane basis for selective vaccine failure: live malaria parasites in the skin inhibit vaccine function. We next show published molecular and cellular data support a testable, novel model where parasite-host interactions in the skin induce malaria-specific regulatory T cells, and subvert early antigen-specific immunity to parasite-specific immunotolerance. This ensures infection and tolerance to reinfection. Exposure to Plasmodium-infected mosquito bites therefore systematically triggers immunosuppression of endemic vaccine-elicited responses. The extensive vaccine trial data solidly substantiate this model experimentally. Conclusions/Significance: We conclude skinstage-initiated immunosuppression, unassociated with bloodstage parasites, systematically blocks vaccine function in the field. Our model exposes novel molecular and procedural strategies to significantly and quickly increase protective efficacy in both pipeline and currently ineffective malaria vaccines, and forces fundamental reassessment of central precepts determining vaccine development. This has major implications fo

Strain differences in the immune response of mice. II. Responses by neonatal cells in irradiated adult hosts.

Lethally irradiated NZB and C57BL mice were injected with syngeneic thymus and marrow, or thymus and liver cells, and immunized with sheep red blood cells (SRBC). As in intact neonatal mice, NZB plaque-forming cell (PFC) responses were significantly higher than C57BL. Irradiated (NZB×C57BL)F(1) and (NZB×BALB/c)F(1) hybrid mice were given mixtures of parental and syngeneic cells, and it was shown that the high NZB response to SRBC was characteristic of the newborn liver rather than of the thymus. NZB liver gave rise to more PFC against SRBC than BALB/c liver, but not more against chicken RBC. It is argued that liver cells contain genetic information regarding antibody specificity. C57BL cells grew poorly in F(1) hosts, but the low SRBC response appeared to be characteristic of both liver and thymus. The nomenclature of the participating cells, and their role in the development of immunological responsiveness, are discussed

Hypoglycemia and Hyperinsulinemia in Rodent Models of Severe Malaria Infection

Severe hypoglycemia developed during nonlethal Plasmodium chabaudi and lethal P. yoelii blood stage malaria infection in mice, always in association with hyperinsulinemia. Supernatants of lethal P. yoelii incubated overnight induced hypoglycemia and hyperinsulinemia in normal mice. In murine malaria, hypoglycemia may be largely secondary to increased insulin secretion