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Henrich J Boyd R McElreath R Gurven M Richerson PJ Ensminger J Alvard M Barr A Barrett C Bolyanatz A Camerer CF Cardenas JC Fehr E Gintis HM Gil-White F Gwako EL Henrich N Hill K Lesorogol C Patton JQ Marlowe FW Tracer DP Ziker J 《Proceedings of the National Academy of Sciences of the United States of America》2012,109(2):E32-3; author reply E34
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Archin NM Vaidya NK Kuruc JD Liberty AL Wiegand A Kearney MF Cohen MS Coffin JM Bosch RJ Gay CL Eron JJ Margolis DM Perelson AS 《Proceedings of the National Academy of Sciences of the United States of America》2012,109(24):9523-9528
HIV type 1 (HIV-1) persists within resting CD4(+) T cells despite antiretroviral therapy (ART). To better understand the kinetics by which resting cell infection (RCI) is established, we developed a mathematical model that accurately predicts (r = 0.65, P = 2.5 × 10(-4)) the initial frequency of RCI measured about 1 year postinfection, based on the time of ART initiation and the dynamic changes in viremia and CD4(+) T cells. In the largest cohort of patients treated during acute seronegative HIV infection (AHI) in whom RCI has been stringently quantified, we found that early ART reduced the generation of latently infected cells. Although RCI declined after the first year of ART in most acutely infected patients, there was a striking absence of decline when initial RCI frequency was less than 0.5 per million. Notably, low-level viremia was observed more frequently as RCI increased. Together these observations suggest that (i) the degree of RCI is directly related to the availability of CD4(+) T cells susceptible to HIV, whether viremia is controlled by the immune response and/or ART; and (ii) that two pools of infected resting CD4(+) T cells exist, namely, less stable cells, observable in patients in whom viremia is not well controlled in early infection, and extremely stable cells that are established despite early ART. These findings reinforce and extend the concept that new approaches will be needed to eradicate HIV infection, and, in particular, highlight the need to target the extremely small but universal, long-lived latent reservoir. 相似文献
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Ashley E. Walther Sujit K. Mohanty Bryan Donnelly Abigail Coots Monica McNeal Gregory M. Tiao 《The Journal of surgical research》2013
Background
Biliary atresia (BA) is a unique neonatal disease resulting from inflammatory and fibrosing obstruction of the extrahepatic biliary tree. Previous studies have demonstrated the critical role of innate immunity and the Th1 response to activated inflammatory cells and overexpressed cytokines in the pathogenesis of BA. Myeloid differentiation factor 88 (MyD88) is a critical adaptor molecule that has been shown to play a crucial role in immunity. We investigated the role of MyD88 in the inflammatory response and development of cholangiopathy in murine BA.Methods
MyD88 knockout (MyD88−/−) and wild-type (WT) BALB/c pups were injected with Rhesus rotavirus or saline on day 1 of life. The mice were monitored for clinical symptoms of BA, including jaundice, acholic stools, bilirubinuria, and death. The liver and extrahepatic bile ducts were harvested for histologic evaluation and the quantification of viral content, determination of cytokine expression, and detection of inflammatory cells.Results
Rhesus rotavirus infection produced symptoms in 100% of both MyD88−/− and WT pups, with survival of 18% of WT and 0% of MyD88−/− mice. Histologic analysis demonstrated bile duct obstruction in both MyD88−/− and WT mice. Viral titers obtained 7 d after infection and expression of interferon-γ and tumor necrosis factor-α at day 3, 5, 8, and 12 after infection revealed no significant differences between the WT and MyD88−/− mice. Flow cytometry demonstrated similar levels of activated CD8+ T cells and natural killer cells.Conclusions
The pathogenesis of murine BA is independent of the MyD88 signaling inflammatory pathway, suggesting alternative mechanisms are crucial in the induction of the model. 相似文献78.
Schwenter F Faughnan ME Gradinger AB Berk T Gryfe R Pollett A Cohen Z Gallinger S Durno C 《Journal of gastroenterology》2012,47(7):795-804
Background
Hereditary hemorrhagic telangiectasia (HHT) is an autosomal dominant disorder most often caused by mutation in the endoglin or ALK1 genes. A distinct syndrome combines the clinical features of HHT and juvenile polyposis (JP) and has been associated with SMAD4 mutation. The aim of this study was to describe the phenotype of patients with JP–HHT and SMAD4 mutations and to compare this phenotype with HHT or JP patients with mutations other than SMAD4.Methods
Patients prospectively enrolled in the Toronto HHT and JP databases who underwent genotyping were included. The phenotypic characteristics of JP–HHT patients with SMAD4 mutations and patients with mutations other than SMAD4 were analyzed and compared.Results
Three hundred and fifty-eight patients underwent genetic testing (HHT, n?=?332; JP, n?=?26). Among fourteen patients identified with SMAD4 mutations, ten met the clinical diagnostic criteria for both JP and HHT (71%). Patients with SMAD4 mutations had 100% penetrance of the polyposis phenotype. All patients with JP and SMAD4 mutation had features of HHT. Three JP–HHT patients developed early onset colorectal cancer (CRC) (mean age 28 years). JP–HHT patients with SMAD4 mutation had a significantly higher rate of anemia than HHT patients with mutations other than SMAD4.Conclusions
Patients with HHT and SMAD4 mutations are at significant risk of JP and CRC. The gastrointestinal phenotype is similar to JP patients without SMAD4 mutation. It is essential for HHT patients to undergo genetic testing to determine if they have SMAD4 mutations so that appropriate gastrointestinal screening and surveillance for JP and CRC can be completed. 相似文献79.
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Elizabeth FitzSullivan MD Sara A. Lari BS Benjamin Smith MD Abigail S. Caudle MD Savitri Krishnamurthy MD Anthony Lucci MD Elizabeth A. Mittendorf MD PhD Gildy V. Babiera MD Dalliah M. Black MD Jamie L. Wagner DO Isabelle Bedrosian MD Wendy Woodward MD Sarah M. Gainer MD Rosa Hwang MD Funda Meric-Bernstam MD Kelly K. Hunt MD Henry M. Kuerer MD PhD 《Annals of surgical oncology》2013,20(13):4103-4112