Poverty, Educational Attainment and Health Among America’s Children: Current and Future Effects of Population Diversification and Associated Socioeconomic Change

A complex of interrelated factors including minority status, poverty, education, health status, and other factors determine the general welfare of children in America, particularly in heavily diverse states such as Texas. Although racial/ethnic status is clearly only a concomitant factor in that determination it is a factor for which future projections are available and for which the relationships with the other factors in the complex can be assessed. After examining the nature of the interrelationships between these factors we utilize direct standardization techniques to examine how the future diversification of the United States and Texas will affect the number of children in poverty, the educational status of the householders in households in which children in poverty live and the health status of children in 2040 assuming that the current relationships between minority status and these socioeconomic factors continue into the future. In the results of the analyses, data are compared with the total population of the United States and Texas in 2040 assumed in the first simulation scenario, to have the race/ethnicity characteristics of 2008 and in the second those projected for 2040 by the U.S. Census Bureau for the nation and by the Texas State Data Center for Texas in 2040. The results show that the diversification of the population could increase the number of children in poverty in the United States by nearly 1.8 million more than would occur with the lower levels of diversification evident in 2008. In addition, poverty would become increasingly concentrated among minority children with minority children accounting for 76.2 percent of all children in poverty by 2040 and with Hispanic children accounting for nearly half of the children in poverty by 2040. Results for educational attainment show an increasing concentration of minority children in households with householders with very low levels of education such that by 2040, 85.2 percent of the increase in the number of children in poverty would be in households with a householder with less than a high school level of education. Finally, the results related to several health status factors show that children in poverty will have a higher prevalence of nearly all health conditions. For example, the number of children with untreated dental conditions could increase to more than 4 million in the United States and to nearly 500,000 in Texas. The results clearly show that improving the welfare of children in America will require concerted efforts to change the poverty, educational, and health status characteristics associated with minority status and particularly Hispanic status. Failing to do so will lead to a future in which America’s children are increasingly impoverished, more poorly educated, and less healthy and which, as a result, is an America with a more tentative future.

The role of the conserved N -terminal domain of STAT3 in STAT3 dephosphorylation and nuclear export

Rapid redistribution of STAT subcellular localization is an essential feature of cytokine signaling. To elucidate the molecular basis of STAT3 function, which plays a critical role in controlling innate immune responses in vivo, we initiated studies to determine the mechanisms controlling STAT3 nuclear trafficking. We found that STAT3 is transported to the nucleus in the absence of cytokine treatment, as judged by indirect immunofluorescence studies in the presence of leptomycin B, an inhibitor of CRM1-dependent nuclear export, suggesting that the non-phosphorylated STAT3 protein contains a functional nuclear import signal. An isoform lacking the STAT3 N-terminal domain (Δ133STAT3) retains the ability to undergo constitutive nuclear localization, indicating that this region is not essential for cytokine-independent nuclear import. Δ133STAT3 is also transported to the nucleus following stimulation with interleukin-6 (IL-6). Interestingly, IL-6-dependent tyrosine phosphorylation of Δ133STAT3 appears to be prolonged and the nuclear export of the protein delayed in cells expressing endogenous STAT3, consistent with defective Δ133STAT3 dephosphorylation. Endogenous STAT3 does not promote the nuclear export of Δ133STAT3, although dimerization between endogenous Stat3 and Δ133STAT3 is detected readily. Thus, the STAT3 N-terminal domain is not required for dimerization with full-length STAT3, yet appears to play a role in proper export of Stat3 from the nucleus following cytokine stimulation. STAT3-deficient cells reconstituted with Δ133STAT3 show enhanced and prolonged Stat1 signaling in response to IL-6, suggesting that induction of the STAT3-dependent negative regulator SOCS3 is impaired. In fact, Δ133STAT3 fails to induce SOCS3 mRNA efficiently. These studies collectively indicate that the STAT3 N-terminal region may be important for IL-6-dependent target gene activation and nuclear dephosphorylation, while dispensable for nuclear import. STAT3 is an oncogene. STAT3 is constitutively activated in primary tumors of many types. Thus far, research in the design of STAT3 protein inhibitors has focused on the SH2 and DNA-binding domains of STAT3. Interference with these domains eliminates all signaling through STAT3. If the N-terminal domain is involved in tetramerization on a subset of target genes, inhibition of this region may lead to a more selective inhibition of some STAT3 functions while leaving others intact. ^