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1.
Rural Policy Brief ; 2018(4): 1-4, 2018 Aug 01.
Article in English | MEDLINE | ID: mdl-30211516

ABSTRACT

Purpose: This RUPRI Center data report describes Medicare accountable care organization (ACO) growth in non-metropolitan U.S. counties from 2016 to 2017. This data report, which includes data through December 2017, follows a similar analysis released in October 2016 that described ACO trends from 2013 to 2015. Key Findings: The following findings are based on activity through 2017: (1) Medicare ACOs operate (an ACO provider is present) in 60.3 percent of all nonmetropolitan counties, up from 41.8 percent in 2016, (2) As of December 2017, no nonmetropolitan ACOs were participating in ACO models that included downside risk (meaning they are liable for expenditures exceeding a benchmark).


Subject(s)
Accountable Care Organizations/statistics & numerical data , Medicare/statistics & numerical data , Rural Health Services/supply & distribution , Accountable Care Organizations/trends , Forecasting , Humans , Medicare/trends , Rural Health Services/statistics & numerical data , Rural Population , United States
2.
J Virol ; 85(22): 11615-25, 2011 Nov.
Article in English | MEDLINE | ID: mdl-21900173

ABSTRACT

Late in infection herpesviruses move DNA-filled capsids from the nucleus to the cytoplasm by enveloping DNA-containing capsids at the inner nuclear membrane (INM) and deenveloping them at the outer nuclear membrane. This process requires two conserved herpesvirus proteins, pUL31 and pUL34. Interaction between pUL34 and pUL31 is essential for targeting both proteins to the nuclear envelope (NE), and sequences that mediate the targeting interaction have been mapped in both proteins. Here, we show that a mutation in the INM-targeting domain of pUL34 fails to support production of infectious virus or plaque formation. The mutation results in multiple defects, including impaired interaction between pUL34 and pUL31, poor NE targeting of pUL34, and misregulated, capsid-independent budding of the NE. The mutant defects in virus production, plaque formation, and pUL31 interaction can be suppressed by other mutations in the INM-targeting domain of pUL31 and by additional mutations in the pUL34 coding sequence.


Subject(s)
Herpesvirus 1, Human/genetics , Herpesvirus 1, Human/pathogenicity , Nuclear Envelope/virology , Suppression, Genetic , Viral Proteins/genetics , Viral Proteins/metabolism , Virus Release , Animals , Cell Membrane/metabolism , Chlorocebus aethiops , Nuclear Envelope/metabolism , Nuclear Proteins/genetics , Protein Binding , Protein Interaction Domains and Motifs , Protein Interaction Mapping , Vero Cells , Viral Plaque Assay
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