Mapping Lyme Disease Incidence for Diagnostic and Preventive Decisions, Maryland

To support diagnostic and preventive decision making, we analyzed incidence of Lyme disease in Maryland on the zip code level. Areas of high incidence were identified on the Upper Eastern Shore of the Chesapeake Bay and in counties north and east of Baltimore City. These latter foci, especially, are not visible when mapping Lyme disease on the county level.

p53 Activation following Rift Valley Fever Virus Infection Contributes to Cell Death and Viral Production

Rift Valley fever virus (RVFV) is an emerging viral zoonosis that is responsible for devastating outbreaks among livestock and is capable of causing potentially fatal disease in humans. Studies have shown that upon infection, certain viruses have the capability of utilizing particular cellular signaling pathways to propagate viral infection. Activation of p53 is important for the DNA damage signaling cascade, initiation of apoptosis, cell cycle arrest and transcriptional regulation of multiple genes. The current study focuses on the role of p53 signaling in RVFV infection and viral replication. These results show an up-regulation of p53 phosphorylation at several serine sites after RVFV MP-12 infection that is highly dependent on the viral protein NSs. qRT-PCR data showed a transcriptional up-regulation of several p53 targeted genes involved in cell cycle and apoptosis regulation following RVFV infection. Cell viability assays demonstrate that loss of p53 results in less RVFV induced cell death. Furthermore, decreased viral titers in p53 null cells indicate that RVFV utilizes p53 to enhance viral production. Collectively, these experiments indicate that the p53 signaling pathway is utilized during RVFV infection to induce cell death and increase viral production

The James Webb Space Telescope Mission

Twenty-six years ago a small committee report, building on earlier studies, expounded a compelling and poetic vision for the future of astronomy, calling for an infrared-optimized space telescope with an aperture of at least $4m$. With the support of their governments in the US, Europe, and Canada, 20,000 people realized that vision as the $6.5m$ James Webb Space Telescope. A generation of astronomers will celebrate their accomplishments for the life of the mission, potentially as long as 20 years, and beyond. This report and the scientific discoveries that follow are extended thank-you notes to the 20,000 team members. The telescope is working perfectly, with much better image quality than expected. In this and accompanying papers, we give a brief history, describe the observatory, outline its objectives and current observing program, and discuss the inventions and people who made it possible. We cite detailed reports on the design and the measured performance on orbit.Comment: Accepted by PASP for the special issue on The James Webb Space Telescope Overview, 29 pages, 4 figure

Gene Frequency Clines Produced by Kin-Structured Founder Effects

Two mechanisms are commonly invoked to explain geographic gradients in gene frequencies (clines): gene flow and natural selection. Thus gene frequency clines in Europe have been attributed to gene flow because expanding Neolithic farmers from the Near East spread and absorbed resident foragers, a process Cavalli-Sforza and his colleagues labeled demic diffusion. Alternatively, gradients in natural selection can produce the same genetic pattern. A third mechanism to explain European clines has recently been proposed by Barbujani et al. (1995). They found that European allele frequencies were consistent with distributions generated by a simple model of total replacement of foragers by expanding farmers. Clines were produced by repeated founder effects in colonizing farmer groups. Here, I present a simulation model using different population parameters to test the generality of the Barbujani model. Results of the simulation show that steep clines (measured by spatial autocorrelation statistics) can be produced by kin-structured founder effects. The implication of these findings is that several genetic mechanisms are consistent with the allele distributions in Europe. To discriminate among these alternatives, other information, such as better archeological and demographic characterization of interactions between farmers and foragers, is required. In any case, the mere presence of genetic clines does not necessarily validate the demic diffusion model

Colonization Models and Initial Genetic Diversity in the Americas

The mode and tempo of colonization of the Americas established the initial pattern of continental genetic diversity. Despite a long history of study, the process of settlement remains controversial in terms of date, rate, and pattern. While there is agreement that Asia was the source population, several different models have been proposed for the colonization process. A classic model postulates a rapid spread of population (“blitzkrieg”) from a small band of hunters entering through the corridor between the continental ice sheets circa 11,000 years b.p. Colonization occurred as a wave of expansion across the land masses of North and South America. An alternative model envisions the original colonists initially limiting settlement to the coastline, using boats, and entering the Americas at an earlier date, circa 13,500 b.p. Range expansion along this linear habitat from North to South America could be rapid without requiring population saturation of entire continental regions. These models have markedly different implications for genetic variation among Native Americans. The blitzkrieg colonization process would have generated multiple founder effects leading to extreme loss of genetic variation. Computer simulation of this model shows nearly complete fixation in 30 generations. Simulation of the coastal model, on the other hand, requires less extreme demographic assumptions and maintains substantial genetic variability after 100 generations. Although with the coastal model continental interiors are occupied less rapidly than with the blitzkrieg model, the coastal model allows earlier entry and rapid expansion to the southern limits of the hemisphere

Changing Sex Ratio of Mortality in the Semai Senoi, 1969-1987

An excess of male over female deaths is characteristic of modem national populations, whereas in some high-mortality societies female mortality exceeds that of males. Among the Semai Senoi, a Malaysian Orang Asli (“aboriginal”) population, women experienced higher mortality than males in the decades before 1969. This differential occurred in all age classes older than 15 years so that the sex ratio progressively increased with age. A recent (1987) restudy of the Semai population found that sex-specific differential mortality is much reduced. A comparison of the 1969 and 1987 life tables shows a sharp shift in the sex ratios of mortality for the post-15-yearold age classes (the geometric means of age classes 15-44 were 0.768 in 1969 and 0.997 in 1987) so that male and female expectations of further life at age 15 are now nearly identical. In contrast to the best-known cases of high female mortality (mostly in South Asia), Semai sex differential mortality does not include the childhood ages. The Semai have traditionally been relatively sexually egalitarian, and sex bias in care has not occurred. Analysis of sex-specific causes of death for the pre-1969 population suggests that maternal mortality is the major cause of the excess female deaths. The reduced number of maternal deaths seems largely due to better health care, particularly the availability of hospital services. Interestingly, the reduction in female mortality has occurred simultaneously with increased fertility, and overall mortality has continued at relatively high levels (e0 \u3c 36). Thus, rather than forming a component of a unitary demographic transition, declining sex differences in mortality can be accounted for by a specific factor, better maternal care