Global health and local poverty: rich countries' responses to vulnerable populations.

Poverty is an important determinant of ill health, mortality and suffering across the globe. This commentary asks what we can learn about poverty by looking at the way rich countries respond to the needs of vulnerable populations both within their own societies and those of low-income countries. Taking advantage of recent efforts to redefine child poverty in a way that is consistent with the World Health Organization's Commission on Social Determinants of Health, three sets of data are reviewed: levels of child well-being within 23 Organization of Economic Community Development countries; the amount of official development assistance these countries disburse to poor countries; and, government social transfers targeted at families as a percentage of GDP. Analysis shows that countries in Northern Europe tend to have lower levels of child poverty, and are the most generous with social transfers and providing development assistance to poor countries; in contrast, the non-European countries like Australia, Canada, Japan, and the United States, and generally, the G7 countries, are the least generous towards the vulnerable at home and abroad and tend to have the highest levels of child poverty. The findings suggest that nations' responses tend to be ideologically based rather than evidence or needs based and that poverty is neither inevitable nor intractable.

Sub-Saharan Africa's HIV pandemic.

Longitudinal studies and household surveys suggest that sub-Saharan Africa's (SSA's) HIV/AIDS crisis is not a pandemic of the poor but rather one of inequalities, where wealthier individuals are more likely to be infected as a result of greater mobility and multiple relationships (Fox, 2012). This is in sharp contrast to the situation in the United States, where HIV infections "are concentrated among the poor with very few people in the middle and upper social strata contracting HIV" (Pellowski, Kalichman, Matthews, & Adler, May-June 2013, p. 199). Yet from a global perspective, wherein SSA is the poorest region in the world, the pandemic is of course one of poverty as well as one with pronounced racial and gender disparities. Both the May-June 2013 special issue of the American Psychologist ("HIV/AIDS: Social Determinants and Health Disparities") and another American Psychologist special issue 25 years earlier ("Psychology and AIDS," November 1988) help shed light on Africa's HIV/AIDS crisis.

In vitro studies on the lymphoma growth-inhibitory activity of sulfasalazine.

Sulfasalazine (SASP) is a novel, potent inhibitor of cellular cystine uptake mediated by the x(c)- cystine/glutamate antiporter. Lymphoid cells cannot synthesize cyst(e)ine and depend for growth on its uptake from their micro-environment. We previously showed that SASP (0.2 mM) can abrogate lymphoma cell proliferation in vitro by specifically inhibiting x(c)- -mediated cystine uptake. Intraperitoneal administration of SASP to Noble rats markedly suppressed Nb2-U17 rat lymphoma transplant growth, notably without major toxicity to the hosts. Since Nb2-U17 cells are x(c)- -deficient, the growth arrest was apparently not due to SASP-tumor cell interaction, but possibly to interference with x(c)- -mediated cysteine secretion by somatic cells. In this study we found that replication of x(c)- -deficient Nb2-11 lymphoma cells can be sustained in vitro, in the absence of cystine uptake enhancers, by co-culturing with IMR-90 fibroblasts known to secrete cysteine. SASP, at 0.15 and 0.2 mM, arrested replication of fibroblast-driven Nb2-11 cells by 93 and 100%, respectively, without impeding fibroblast proliferation. Addition of 2-mercapto-ethanol (60 microM), a cystine uptake enhancer, almost completely prevented this growth arrest, indicating that SASP specifically inhibited cysteine secretion by the fibroblasts, a process based on x(c)- -mediated cystine uptake. It is proposed that the lymphoma growth-inhibitory activity of SASP in vivo involves inhibition of cysteine secretion by tumor-associated somatic cells (macrophages, dendritic cells), leading to cysteine starvation of the tumor cells and apoptosis. The difference between the lymphoma cells and fibroblasts in sensitivity to SASP treatment is consistent with the marked antitumor effect of SASP lacking significant side effects.