Why do nominal characteristics acquire status value? A minimal explanation for status construction.

Why do beliefs that attach different amounts of status to different categories of people become consensually held by the members of a society? We show that two microlevel mechanisms, in combination, imply a system-level tendency toward consensual status beliefs about a nominal characteristic. (1) Status belief diffusion: a person who has no status belief about a characteristic can acquire a status belief about that characteristic from interacting with one or more people who have that status belief. (2) Status belief loss: a person who has a status belief about a characteristic can lose that belief from interacting with one or more people who have the opposite status belief. These mechanisms imply that opposite status beliefs will tend to be lost at equal rates and will tend to be acquired at rates proportional to their prevalence. Therefore, if a status belief ever becomes more prevalent than its opposite, it will increase in prevalence until every person holds it.

Adolescent weight status and self-reported school performance in South Korea.

Using a nationally representative sample of 142 783 middle school (13-15 years old) and high school (16-18 years old) students in South Korea, this study examined whether (1) overweight and obesity are more likely to be associated with lower self-reported school performance; (2) overweight and obese students are more likely to enrol in a vocational high school as opposed to a general high school; (3) the association between obesity and poorer self-reported school performance is mediated through body image stress and health status. We found that excess weight was negatively associated with self-reported school performance among middle and general high school students, and that obese students had a higher probability of being enrolled in a vocational over a general high school. We did not find strong evidence on the mediating role of body image stress and health status.

Socio-economic status and malaria-related outcomes in Mvomero District, Tanzania.

While policies often target malaria prevention and treatment - proximal causes of malaria and related health outcomes - too little attention has been given to the role of household- and individual-level socio-economic status (SES) as a fundamental cause of disease risk in developing countries. This paper presents a conceptual model outlining ways in which SES may influence malaria-related outcomes. Building on this conceptual model, we use household data from rural Mvomero, Tanzania, to examine empirical relationships among multiple measures of household and individual SES and demographics, on the one hand, and malaria prevention, illness, and diagnosis and treatment behaviours, on the other. We find that access to prevention and treatment is significantly associated with indicators of households' wealth; education-based disparities do not emerge in this context. Meanwhile, reported malaria illness shows a stronger association with demographic variables than with SES (controlling for prevention). Greater understanding of the mechanisms through which SES and malaria policies interact to influence disease risk can help to reduce health disparities and reduce the malaria burden in an equitable manner.

Use of "entertainment" chimpanzees in commercials distorts public perception regarding their conservation status.

Chimpanzees (Pan troglodytes) are often used in movies, commercials and print advertisements with the intention of eliciting a humorous response from audiences. The portrayal of chimpanzees in unnatural, human-like situations may have a negative effect on the public's understanding of their endangered status in the wild while making them appear as suitable pets. Alternatively, media content that elicits a positive emotional response toward chimpanzees may increase the public's commitment to chimpanzee conservation. To test these competing hypotheses, participants (n = 165) watched a series of commercials in an experiment framed as a marketing study. Imbedded within the same series of commercials was one of three chimpanzee videos. Participants either watched 1) a chimpanzee conservation commercial, 2) commercials containing "entertainment" chimpanzees or 3) control footage of the natural behavior of wild chimpanzees. Results from a post-viewing questionnaire reveal that participants who watched the conservation message understood that chimpanzees were endangered and unsuitable as pets at higher levels than those viewing the control footage. Meanwhile participants watching commercials with entertainment chimpanzees showed a decrease in understanding relative to those watching the control footage. In addition, when participants were given the opportunity to donate part of their earnings from the experiment to a conservation charity, donations were least frequent in the group watching commercials with entertainment chimpanzees. Control questions show that participants did not detect the purpose of the study. These results firmly support the hypothesis that use of entertainment chimpanzees in the popular media negatively distorts the public's perception and hinders chimpanzee conservation efforts.

The impact of host immune status on the within-host and population dynamics of antigenic immune escape.

Antigenically evolving pathogens such as influenza viruses are difficult to control owing to their ability to evade host immunity by producing immune escape variants. Experimental studies have repeatedly demonstrated that viral immune escape variants emerge more often from immunized hosts than from naive hosts. This empirical relationship between host immune status and within-host immune escape is not fully understood theoretically, nor has its impact on antigenic evolution at the population level been evaluated. Here, we show that this relationship can be understood as a trade-off between the probability that a new antigenic variant is produced and the level of viraemia it reaches within a host. Scaling up this intra-host level trade-off to a simple population level model, we obtain a distribution for variant persistence times that is consistent with influenza A/H3N2 antigenic variant data. At the within-host level, our results show that target cell limitation, or a functional equivalent, provides a parsimonious explanation for how host immune status drives the generation of immune escape mutants. At the population level, our analysis also offers an alternative explanation for the observed tempo of antigenic evolution, namely that the production rate of immune escape variants is driven by the accumulation of herd immunity. Overall, our results suggest that disease control strategies should be further assessed by considering the impact that increased immunity--through vaccination--has on the production of new antigenic variants.

HPV16 antibodies as risk factors for oropharyngeal cancer and their association with tumor HPV and smoking status.

BACKGROUND: Antibodies (Abs) to the HPV16 proteome increase risk for HPV-associated OPC (HPVOPC). The goal of this study was to investigate the association of a panel of HPV16 Abs with risk for OPC as well as the association of these Abs with tumor HPV and smoking status among patients with OPC. METHODS: IgG Abs to the HPV16 antigens E1, E2, E4, E5, E6, E7, L1, L2 were quantified using a programmable ELISA assay. Sera were obtained from 258 OPC patients at diagnosis and 250 healthy controls. HPV16 tumor status was measured by PCR for 137 cases. Multivariable logistic regression was used to calculate odds ratios for the association of HPV16 Abs with risk for OPC. RESULTS: HPV16 E1, E2, E4, E5, E6, E7 and L1-specific IgG levels were elevated in OPC patients compared to healthy controls (p<0.05). After multivariable adjustment, Ab positivity for NE2, CE2, E6, and/or E7 was associated with OPC risk (OR [95% CI], 249.1 [99.3-624.9]). Among patients with OPC, Ab positivity for these antigens was associated with tumor HPV status, especially among never or light smokers (OR [95% CI], 6.5 [2.1-20.1] and OR [95% CI], 17.5 [4.0-77.2], respectively). CONCLUSIONS: Antibodies to HPV16 proteins are associated with increased risk for HPVOPC. Among patients with OPC, HPV16 Abs are associated with tumor HPV status, in particular among HPV positive patients with no or little smoking history.

Increased leptin levels correlate with thyroid autoantibodies in nonobese males.

OBJECTIVE: Leptin is an adipokine that regulates body weight and appetite. It is also an inflammatory cytokine that influences immune reactivity and autoimmunity. Leptin levels are increased in obesity and are higher in women than in men. We aimed to determine whether leptin levels, independent of sex and body mass index (BMI), are associated with thyroid autoimmunity. DESIGN: This study uses data from The Third National Health and Nutrition Examination Survey (NHANES III) to test the association of leptin and thyroid autoimmunity, independent of BMI. MEASUREMENTS: Thyroid-stimulating hormone, thyroxine, antithyroid peroxidase (TPO) antibodies and leptin levels were measured in 2902 men and 3280 women within the NHANES III population. BMI was calculated from height and weight. RESULTS: Women had significantly higher leptin levels and anti-TPO antibody titres than men. Correlation analyses demonstrated that leptin levels were associated with anti-TPO antibody levels in the total population, but when men and women were analysed separately, this association was lost. We then stratified men and women into obese (BMI > 30) or nonobese (BMI ≤ 30) subgroups and determined the association between leptin levels and anti-TPO antibody titres for each subgroup. Using regression analysis, we found that increased leptin levels correlated with thyroid autoantibodies in nonobese males, but not in obese males or in females. CONCLUSIONS: Leptin levels correlated with thyroid autoantibody titres in nonobese males. This association was not found in females. Sex and body habitus should therefore be considered in studying the role of leptin in other autoimmune conditions.

A Peptide Uncoupling BDNF Receptor TrkB from Phospholipase Cγ1 Prevents Epilepsy Induced by Status Epilepticus.

The BDNF receptor tyrosine kinase, TrkB, underlies nervous system function in both health and disease. Excessive activation of TrkB caused by status epilepticus promotes development of temporal lobe epilepsy (TLE), revealing TrkB as a therapeutic target for prevention of TLE. To circumvent undesirable consequences of global inhibition of TrkB signaling, we implemented a novel strategy aimed at selective inhibition of the TrkB-activated signaling pathway responsible for TLE. Our studies of a mouse model reveal that phospholipase Cγ1 (PLCγ1) is the dominant signaling effector by which excessive activation of TrkB promotes epilepsy. We designed a novel peptide (pY816) that uncouples TrkB from PLCγ1. Treatment with pY816 following status epilepticus inhibited TLE and prevented anxiety-like disorder yet preserved neuroprotective effects of endogenous TrkB signaling. We provide proof-of-concept evidence for a novel strategy targeting receptor tyrosine signaling and identify a therapeutic with promise for prevention of TLE caused by status epilepticus in humans.