Background:The platform protein PilC and/or the alignment subcomplex PilMNOP may coordinate type IV pilus (T4P) extension/retraction ATPases. Results: Loss of PilC in a retraction-deficient background abolished assembly. C-terminal mutations were permissive for assembly but not twitching motility. Conclusion: PilC is essential for pilus biogenesis and twitching motility. Significance: Platform proteins are conserved essential components of T4P and type II secretion machines.
Evidence supporting prophylactic swallow exercises for patients with head and neck cancer (HNC) has not been universally demonstrated. This RCT examined diet level, feeding tube use, swallow function, and quality of life (QOL) of patients undergoing chemoradiotherapy who performed prophylactic swallowing exercises. Sixty HNC patients were randomized into exercise versus control groups. Swallowing, oromotor, toxicity, and QOL data were recorded (baseline, 3, 6, 12, 24 months). Physiological swallow function was examined at baseline and 3 months. Swallow exercises were completed twice daily. Oral intake at 3 months was 10% better in the exercise group, which was not statistically significant (p = 0.49). Significant (p < 0.05) differences in secondary outcomes including oromotor function, pharyngeal impairment, oral pharyngeal swallow efficiency, and incisal opening were noted at early time points (3–6 months) in the exercise group. Possible positive early improvements in swallow function are associated with swallowing exercises, although these improvements are not significant longer term.
Aims/hypothesis Adult beta cells have a diminished ability to proliferate. Phosphatase and tensin homologue (PTEN) is a lipid phosphatase that antagonises the function of the mitogenic phosphatidylinositol 3-kinase (PI3K) pathway. The objective of this study was to understand the role of PTEN and PI3K signalling in the maintenance of beta cells postnatally. Methods We developed a Ptenlox/lox; Rosa26lacZ; RIP-CreER+ model that permitted us to induce Pten deletion by treatment with tamoxifen in mature animals. We evaluated islet mass and function as well as beta cell proliferation in 3- and 12-month-old mice treated with tamoxifen (Pten deleted) vs mice treated with vehicle (Pten control). Results Deletion of Pten in juvenile (3-month-old) beta cells significantly induced their proliferation and increased islet mass. The expansion of islet mass occurred concomitantly with the enhanced ability of the Pten-deleted mice to maintain euglycaemia in response to streptozotocin treatment. In older mice (>12 months of age), deletion of Pten similarly increased islet mass and beta cell proliferation. This novel finding suggests that PTEN-regulated mechanisms may override the age-onset diminished ability of beta cells to respond to mitogenic stimulation. We also found that proteins regulating G1/S cell-cycle transition, such as cyclin D1, cyclin D2, p27 and p16, were altered when PTEN was lost, suggesting that they may play a role in PTEN/PI3K-regulated beta cell proliferation in adult tissue. Conclusions/interpretation The signals regulated by the PTEN/PI3K pathway are important for postnatal maintenance of beta cells and regulation of their proliferation in adult tissues.
The law that created Medicare's prescription drug benefit, Medicare Part D, also established extra help for low-income seniors in the form of a subsidy. This study, the first in-depth analysis of Part D enrollment among Medicare beneficiaries without prior drug coverage, finds that 63 percent of all eligible seniors and 69 percent of low-income beneficiaries were enrolled in Part D in 2006. However, only 29 percent of low-income beneficiaries were enrolled in the subsidy program, leaving millions without coverage. Many reported that premiums were too costly, enrollment too difficult, and information too hard to obtain for enrollment. Additionally, provisions of the recently enacted Patient Protection and Affordable Care Act may have the perverse impact of reducing enrollment in Part D for certain beneficiaries. Our findings emphasize the need to expand eligibility and improve policies to foster enrollment.
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