Text4baby Program: An Opportunity to Reach Underserved Pregnant and Postpartum Women?

Text4baby was launched in 2010 to promote healthy pregnancies and babies by the use of text messaging. The primary objective of this study was to assess factors related to the enrollment process and reception of text4baby. A prospective cohort study was conducted in two Women, Infant and Children clinics in Atlanta (April 2010–July 2011). Randomly selected pregnant and postpartum women (n = 468) were queried on cell phone use and instructed on text4baby enrollment. Self-enrollment issues were assessed at one-week follow-up (n = 351, 75.0 %), and message reception and reading patterns at two-month follow-up (n = 209, 44.7 %). Forty-two percent of the women had some college education and 82 % had household income <=$20,000. About half attempted text4baby self-enrollment (162/351), with enrollment success more likely among women with more education (80 % with some college vs. 62 % with less education), with household income above $10,000 (61 % < $10,000 vs. 83 % $10,001-$20,000 and 76 % > $20,000), and among women living in smaller households (77 % 1–3 members vs. 58 % > 3 members) (all p < 0.001). Among the 209 participants in the final follow-up contact, >90 % reported uninterrupted reception and regular reading of messages, and 88 % planned to continue using text4baby. Results also suggested that respondents who were younger (<26 year), less educated and had lower health literacy skills were more likely to have interrupted messages. Despite substantial interest in the text4baby program in an underserved population, innovative ways to help women with significant disadvantages enroll and receive uninterrupted messages are needed.     

Hippocampal asymmetry and sudden unexpected death in infancy: a case report

The differential diagnosis of known entities associated with sudden unexpected death in infancy is ever expanding. Here we report the case of a 10-month-old infant boy whose clinical presentation mimicked that of the sudden infant death syndrome (SIDS). This presentation included the typical features of SIDS: sleep-related death; prone position upon discovery; and minor illness within 2?days of death. Nevertheless, neuropathologic examination revealed striking hippocampal asymmetry and microdysgenesis similar to that reported previously by us in toddlers with sleep-related sudden death. Hippocampal maldevelopment in the setting of sudden death in infants and toddlers is analogous to sudden unexpected death in epilepsy associated with temporal lobe pathology, and suggests a possible role for seizures in the terminal events leading to sudden death. This report serves to alert pediatric and forensic pathologists to hippocampal asymmetry and microdysgenesis in the differential diagnosis of sudden infant death mimicking SIDS.     

Regional Differences and Tribal Use of American Indian/Alaska Native Cancer Data in the Pacific Northwest

In the Pacific Northwest, cancer is a leading cause of morbidity and mortality for American Indians and Alaska Natives (AI/AN). Misclassification of AI/AN race in state cancer registries causes cancer burden to be underestimated. Furthermore, local-level data are rarely available to individual tribes for use in health assessment and program planning. We corrected race coding in the cancer registries of Idaho, Oregon, and Washington using probabilistic record linkage to a file derived from patient registration records from Indian Health Service and a large urban clinic. We calculated cancer incidence and mortality measures by state, comparing AI/AN to non-Hispanic White (NHW) race. Record linkages identified a high prevalence of misclassified race. Differences in AI/AN cancer patterns were identified across the three state region. Compared to NHW, AI/AN experienced disproportionate late stage rates of some screen-detectable cancers. The correct classification of race is a crucial factor in cancer surveillance and can reveal regional differences even within a relatively small area. The availability of local-level cancer data can help inform tribes in appropriate intervention efforts.     

Elucidation of the mechanism of mitochondrial iron loading in Friedreich's ataxia by analysis of a mouse mutant

We used the muscle creatine kinase (MCK) conditional frataxin knockout mouse to elucidate how frataxin deficiency alters iron metabolism. This is of significance because frataxin deficiency leads to Friedreich''s ataxia, a disease marked by neurologic and cardiologic degeneration. Using cardiac tissues, we demonstrate that frataxin deficiency leads to down-regulation of key molecules involved in 3 mitochondrial utilization pathways: iron-sulfur cluster (ISC) synthesis (iron-sulfur cluster scaffold protein1/2 and the cysteine desulferase Nfs1), mitochondrial iron storage (mitochondrial ferritin), and heme synthesis (5-aminolevulinate dehydratase, coproporphyrinogen oxidase, hydroxymethylbilane synthase, uroporphyrinogen III synthase, and ferrochelatase). This marked decrease in mitochondrial iron utilization and resultant reduced release of heme and ISC from the mitochondrion could contribute to the excessive mitochondrial iron observed. This effect is compounded by increased iron availability for mitochondrial uptake through (i) transferrin receptor1 up-regulation, increasing iron uptake from transferrin; (ii) decreased ferroportin1 expression, limiting iron export; (iii) increased expression of the heme catabolism enzyme heme oxygenase1 and down-regulation of ferritin-H and -L, both likely leading to increased “free iron” for mitochondrial uptake; and (iv) increased expression of the mammalian exocyst protein Sec15l1 and the mitochondrial iron importer mitoferrin-2 (Mfrn2), which facilitate cellular iron uptake and mitochondrial iron influx, respectively. Our results enable the construction of a model explaining the cytosolic iron deficiency and mitochondrial iron loading in the absence of frataxin, which is important for understanding the pathogenesis of Friedreich''s ataxia.     

Irs2 Inactivation Suppresses Tumor Progression in Pten+/− Mice

Mutations in the phosphatase and tensin homologue (PTEN)/phosphatidylinositol-3 kinase-α (PI3K) signaling pathway are frequently found in human cancer. In addition, Pten^+/− mice develop tumors in multiple organs because of the activation of the PI3K signaling cascade. Because activation of PI3K signaling leads to feedback inhibition of insulin receptor substrate-2 (IRS2) expression, an upstream activator of PI3K, we therefore anticipated that IRS2 expression would be low in tumors that lack PTEN. Surprisingly, however, an elevation of IRS2 was often detected in tumor samples in which PTEN levels were compromised. To determine the potential contribution of Irs2 to tumor progression, Pten^+/− mice were crossed with Irs2^+/− mice. Deletion of Irs2 did not affect the initiation of neoplasia found in Pten^+/− mice but suppressed cancer cell growth, proliferation, and invasion through the basement membrane. Deletion of Irs2 also attenuated the expression of Myc in prostatic intraepithelial neoplasia in Pten^+/− mice. In addition, the expression levels of IRS2 and MYC were highly correlated in human prostate cancer, and IRS2 could stimulate MYC expression in cultured cells. Our findings provide evidence that the PI3K-activating adaptor Irs2 contributes to tumor progression in Pten^+/− mice by stimulating both Myc and DNA synthesis.