This chapter, written for an anthology on Race and Racism in Rural America, assesses the intersections of race and ethnicity with rurality in relation to higher education access and attainment in the State of New Mexico. New Mexico is one of the nation’s most rural states and is home to a distinct population in terms of race and ethnicity: the greatest percentage Latinx/Hispanic population—right at half and growing fast—and the third smallest population of non-Hispanic whites among all states. Further, more than a tenth of New Mexicans identify as American Indian, the second greatest percentage among the states. The fifth most sparsely populated state in the nation, New Mexico struggles chronically with a lagging economy, high poverty and child poverty rates, and low educational attainment. Against that demographic and economic backdrop, the analysis in this chapter reveals disappointing educational attainment among Hispanic and American Indian students as measured against these groups’ proportion of the state’s broader population, but particularly in relation to New Mexico’s college-aged population. In other words, young Hispanics’ status as a majority does not appear to be a protective factor—or at least not a sufficiently protective one—when it comes to higher educational attainment. American Indian students struggle to an even greater degree, falling far behind both their non-Hispanic white and Hispanic counterparts. Still, being low-income is a bigger risk factor than race or ethnicity when it comes to college preparedness. While rural residents’ education level consistently falls behind that of metropolitan residents, it is impossible to determine the extent to which this is due to a rural brain drain—the phenomenon of young people raised in rural areas who migrate to urban areas to obtain their college degrees and then stay, often because of better economic opportunities. Indeed, the data suggest bleak higher education outcomes for all low-income and rural residents, regardless of race or ethnicity. We attribute this in part to inadequate state funding of public higher education and to a mismatch between how that funding is currently spent, e.g., four-year institutions, merit-based student aid, and how it could be better spent to promote access and attainment for the most vulnerable students. We close the chapter with recommendations for policy makers seeking to achieve equity in education and thus also foster a brighter economic future for the entire state. We emphasize the need for the collection of more nuanced data so that the State of New Mexico can better understand trends and shift resources in ways that will make education access more equitable across race, ethnicity, class, and geography.

Immunity to one of the four dengue virus (DV) serotypes can increase disease severity in humans upon subsequent infection with another DV serotype. Serotype cross-reactive antibodies facilitate DV infection of myeloid cells in vitro by promoting virus entry via Fcγ receptors (FcγR), a process known as antibody-dependent enhancement (ADE). However, despite decades of investigation, no in vivo model for antibody enhancement of dengue disease severity has been described. Analogous to human infants who receive anti-DV antibodies by transplacental transfer and develop severe dengue disease during primary infection, we show here that passive administration of anti-DV antibodies is sufficient to enhance DV infection and disease in mice using both mouse-adapted and clinical DV isolates. Antibody-enhanced lethal disease featured many of the hallmarks of severe dengue disease in humans, including thrombocytopenia, vascular leakage, elevated serum cytokine levels, and increased systemic viral burden in serum and tissue phagocytes. Passive transfer of a high dose of serotype-specific antibodies eliminated viremia, but lower doses of these antibodies or cross-reactive polyclonal or monoclonal antibodies all enhanced disease in vivo even when antibody levels were neutralizing in vitro. In contrast, a genetically engineered antibody variant (E60-N297Q) that cannot bind FcγR exhibited prophylactic and therapeutic efficacy against ADE-induced lethal challenge. These observations provide insight into the pathogenesis of antibody-enhanced dengue disease and identify a novel strategy for the design of therapeutic antibodies against dengue.

Background

A comprehensive assessment of Spanish-speaking breast cancer survivors' (SSBCS) survivorship needs is lacking.

Objective

Assess SSBCS' post-treatment symptom management, psychosocial, and informational needs.

Methods

118 telephone surveys and 25 in-person semi-structured interviews with SSBCS, and semi-structured interviews with 5 support providers and 4 physicians who serve SSBCS from 5 Northern California counties.

Results

Surveys identified the most bothersome (bothered by it in the past month "somewhat/quite a bit/a lot") physical symptoms as: joint pain, fatigue, hot flashes, numbness in hands/feet, and vaginal dryness. The most bothersome emotional symptoms were thoughts of recurrence/new cancers, depression/sadness, anxieties, and stress. Seven themes emerged from interviews: 1) unmet physical symptom management needs; 2) social support from family/friends often ends when treatment is completed; 3) challenges resuming roles; 5) sense of abandonment by health care system when treatment ends; 6) need for formal transition from active treatment to follow-up care; 6) fear of recurrence especially when obtaining follow-up care; and 7) desire for information on late effects of initial treatments and side effects of hormonal treatments. Based on survey and interview results, we present a conceptual framework for survivorship care interventions for SSBCS.

Limitations

Sample may not represent SSBCS' concerns seen outside of Northern California hospitals.

Conclusions

Physical and psychosocial symptoms were common. SSBCS need culturally appropriate survivorship care programs that address symptom management, psychosocial concerns, follow-up care, and healthy lifestyles.

The androgen receptor (AR) signaling inhibitor enzalutamide (enza) is one of the principal treatments for metastatic castration-resistant prostate cancer (CRPC). Several emergent enza clinical resistance mechanisms have been described, including lineage plasticity in which the tumors manifest reduced dependency on the AR. To improve our understanding of enza resistance, herein we analyze the transcriptomes of matched biopsies from men with metastatic CRPC obtained prior to treatment and at progression (n = 21). RNA-sequencing analysis demonstrates that enza does not induce marked, sustained changes in the tumor transcriptome in most patients. However, three patients' progression biopsies show evidence of lineage plasticity. The transcription factor E2F1 and pathways linked to tumor stemness are highly activated in baseline biopsies from patients whose tumors undergo lineage plasticity. We find a gene signature enriched in these baseline biopsies that is strongly associated with poor survival in independent patient cohorts and with risk of castration-induced lineage plasticity in patient-derived xenograft models, suggesting that tumors harboring this gene expression program may be at particular risk for resistance mediated by lineage plasticity and poor outcomes.