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Diana Leticia Coronel-MartÍnez Juliana Park Eduardo López-Medina María Rosario Capeding Andrés Angelo Cadena Bonfanti María Cecilia Montalbán Isabel Ramírez María Liza Antoinette Gonzales Carlos A DiazGranados Betzana Zambrano Gustavo Dayan Stephen Savarino Zhenghong Chen Hao Wang Sunny Sun Matthew Bonaparte Andrey Rojas Jenny Carolina Ramírez Fernando Noriega 《The Lancet infectious diseases》2021,21(4):517-528
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Jared M. Weiss MD Nathan Pennell MD PhD Allison M. Deal MS Daniel Morgensztern MD Daniel S. Bradford MD Jeffrey Crane MD Howard Jack West MD Carrie Lee MD Chad Pecot MD James P. Stevenson MD William Irvin MD Mark Socinski MD Tom Stinchcombe MD Liza C. Villaruz MD Hyman B. Muss MD 《Cancer》2020,126(5):1060-1067
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Andreas Mueller Arne Simon Julia Gillen Verena Schildgen Ramona Liza Tillmann Karl Reiter Oliver Schildgen 《Archives of virology》2009,154(10):1605-1608
The polyomaviruses KI (KIPyV) and WU (WUPyV) have recently been discovered in specimens from patients with respiratory tract
infections. To analyze the frequency and clinical impact in a cohort of pediatric patients in a German University Children’s
Hospital. Nasopharyngeal aspirates or bronchoalveolar lavage specimens of 229 children with acute respiratory tract infection
were screened for KIPyV and WUPyV using polymerase chain reaction-based methods. KIPyV was detected in 2 (0.9%) and WUPyV
in 1 (0.4%) patients, without co-infections with other respiratory viruses but with co-detection of CMV, EBV and HHV 6 in
one immunocompromised patient. Only a very small proportion (1.3%) of positive samples for KIPyV and WUPyV was documented
in this study; the clinical relevance of these viruses remains unclear and requires further evaluation. 相似文献
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Binita?ShahEmail author Nicole?Allen Bhisham?Harchandani Michael?Pillinger Stuart?Katz Steven?P.?Sedlis Christina?Echagarruga Svetlana?Krasnokutsky?Samuels Pajazit?Morina Prabhjot?Singh Liza?Karotkin Jeffrey?S.?Berger 《Inflammation》2016,39(1):182-189
The cardioprotective mechanisms of colchicine in patients with stable ischemic heart disease remain uncertain. We tested varying concentrations of colchicine on platelet activity in vitro and a clinically relevant 1.8-mg oral loading dose administered over 1 h in 10 healthy subjects. Data are shown as median [interquartile range]. Colchicine addition in vitro decreased light transmission platelet aggregation only at supratherapeutic concentrations but decreased monocyte- (MPA) and neutrophil-platelet aggregation (NPA) at therapeutic concentrations. Administration of 1.8 mg colchicine to healthy subjects had no significant effect on light transmission platelet aggregation but decreased the extent of MPA (28 % [22–57] to 22 % [19–31], p?=?0.05) and NPA (19 % [16–59] to 15 % [11–30], p?=?0.01), platelet surface expression of PAC-1 (370 mean fluorescence intensity (MFI) [328–555] to 333 MFI [232–407], p?=?0.02) and P-selectin (351 MFI [269–492] to 279 [226–364], p?=?0.03), and platelet adhesion to collagen (10.2 % [2.5–32.6] to 2.0 % [0.2–9.5], p?=?0.09) 2 h post-administration. Thus, in clinically relevant concentrations, colchicine decreases expression of surface markers of platelet activity and inhibits leukocyte-platelet aggregation but does not inhibit homotypic platelet aggregation. 相似文献
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