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1.
Rural Policy Brief ; 2018(4): 1-4, 2018 Aug 01.
Artigo em Inglês | MEDLINE | ID: mdl-30211516

RESUMO

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).


Assuntos
Organizações de Assistência Responsáveis/estatística & dados numéricos , Medicare/estatística & dados numéricos , Serviços de Saúde Rural/provisão & distribuição , Organizações de Assistência Responsáveis/tendências , Previsões , Humanos , Medicare/tendências , Serviços de Saúde Rural/estatística & dados numéricos , População Rural , Estados Unidos
2.
J Virol ; 85(22): 11615-25, 2011 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-21900173

RESUMO

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.


Assuntos
Herpesvirus Humano 1/genética , Herpesvirus Humano 1/patogenicidade , Membrana Nuclear/virologia , Supressão Genética , Proteínas Virais/genética , Proteínas Virais/metabolismo , Liberação de Vírus , Animais , Membrana Celular/metabolismo , Chlorocebus aethiops , Membrana Nuclear/metabolismo , Proteínas Nucleares/genética , Ligação Proteica , Domínios e Motivos de Interação entre Proteínas , Mapeamento de Interação de Proteínas , Células Vero , Ensaio de Placa Viral
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