The Relationship Between Older Adults' Knowledge of Their Drug Coverage and Medication Cost Problems

To determine whether chronically ill patients have gaps in knowledge about their prescription drug coverage and establish the relationship between gaps and medication cost problems. Design : Nationwide, cross-sectional survey. Setting : Nationwide survey conducted via the Internet. Participants : Three thousand one hundred nineteen adults aged 50 and older (1,400 of whom were aged ≥65) who had prescription drug coverage and at least one chronic illness. Measurements : Patients were asked about features of their drug benefits and whether they had experienced problems due to medication costs in the prior year. Results : Twenty-five percent of respondents reported not knowing their usual prescription copayments, and 41% did not know whether there were caps on their drug coverage. Nonwhite race and lower income were independent risk factors for lack of knowledge about these aspects of pharmacy benefits. Lack of knowledge regarding the limits of coverage was associated with a greater likelihood of cutting back on medication use because of cost pressures, forgoing basic needs because of medication costs, borrowing money to pay for prescriptions, and worrying about medication costs (all P <.05). Conclusion : Many older adults with prescription drug coverage do not know important features of their pharmacy benefits. Racial minorities and those with low incomes may have the greatest difficulty understanding coverage and as a result may be at greatest risk for underusing their benefits. Education about Medicare reforms and other efforts to increase prescription coverage should accompany these policies.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/66286/1/j.1532-5415.2005.00527.x.pd

Complicating the Narrative: Contemporary Appalachian photography as a visual counterpoint

Appalachia has long been portrayed as a destitute place in need of sympathy, pity, and aid on one hand. On the other, a wild, untamable region filled with backwoodsmen and granny witches who shoot first and ask questions later. At the least, the visual construct of Appalachia has made a convenient comparative to gauge one’s own circumstance and lot in life. At least my children don’t look like that. At least my home doesn’t look that bad. At least we don’t talk like that. And so on. It stands to reason that if visuals can be used to construct stereotypes, certainly they can be used to deconstruct those same stereotypes and at the very least, complicate the narrative of Appalachia being all poor, all white, and all rural. Contemporary Appalachian photography as showcased in the Looking at Appalachia project, offers a different perspective on the region, a timelier examination to counter what we have historically been shown, and stands as open invitation to photographers of all skill levels to contribute to the greater visual conversation about place. The project is a democratic approach to photographing the region, is open to anyone, and has four simple guidelines: 1) the work must be made in the ARC defined region, 2) must be the original work of the photographer, 3) must be made in the current calendar year, and 4) must be submitted by midnight, December 31 of the current calendar year

Proximal recolonization by self-renewing microglia re-establishes microglial homeostasis in the adult mouse brain.

Microglia are resident immune cells that play critical roles in maintaining the normal physiology of the central nervous system (CNS). Remarkably, microglia have an intrinsic capacity to repopulate themselves after acute ablation. However, the underlying mechanisms that drive such restoration remain elusive. Here, we characterized microglial repopulation both spatially and temporally following removal via treatment with the colony stimulating factor 1 receptor (CSF1R) inhibitor PLX5622. We show that microglia were replenished via self-renewal, with no contribution from nonmicroglial lineages, including Nestin+ progenitors and the circulating myeloid population. Interestingly, spatial analyses with dual-color labeling revealed that newborn microglia recolonized the parenchyma by forming distinctive clusters that maintained stable territorial boundaries over time, indicating the proximal expansive nature of adult microgliogenesis and the stability of microglia tiling. Temporal transcriptome profiling at different repopulation stages revealed that adult newborn microglia gradually regain steady-state maturity from an immature state that is reminiscent of the neonatal stage and follow a series of maturation programs, including nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) activation, interferon immune activation, and apoptosis. Importantly, we show that the restoration of microglial homeostatic density requires NF-κB signaling as well as apoptotic egress of excessive cells. In summary, our study reports key events that take place from microgliogenesis to homeostasis reestablishment

Microglial NFκB-TNFα hyperactivation induces obsessive-compulsive behavior in mouse models of progranulin-deficient frontotemporal dementia.

Frontotemporal dementia (FTD) is the second most common dementia before 65 years of age. Haploinsufficiency in the progranulin (GRN) gene accounts for 10% of all cases of familial FTD. GRN mutation carriers have an increased risk of autoimmune disorders, accompanied by elevated levels of tissue necrosis factor (TNF) α. We examined behavioral alterations related to obsessive-compulsive disorder (OCD) and the role of TNFα and related signaling pathways in FTD patients with GRN mutations and in mice lacking progranulin (PGRN). We found that patients and mice with GRN mutations displayed OCD and self-grooming (an OCD-like behavior in mice), respectively. Furthermore, medium spiny neurons in the nucleus accumbens, an area implicated in development of OCD, display hyperexcitability in PGRN knockout mice. Reducing levels of TNFα in PGRN knockout mice abolished excessive self-grooming and the associated hyperexcitability of medium spiny neurons of the nucleus accumbens. In the brain, PGRN is highly expressed in microglia, which are a major source of TNFα. We therefore deleted PGRN specifically in microglia and found that it was sufficient to induce excessive grooming. Importantly, excessive grooming in these mice was prevented by inactivating nuclear factor κB (NF-κB) in microglia/myeloid cells. Our findings suggest that PGRN deficiency leads to excessive NF-κB activation in microglia and elevated TNFα signaling, which in turn lead to hyperexcitability of medium spiny neurons and OCD-like behavior