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Stephen R. Quake
Researcher at Stanford University
Publications - 626
Citations - 89247
Stephen R. Quake is an academic researcher from Stanford University. The author has contributed to research in topics: Transcriptome & Biology. The author has an hindex of 132, co-authored 589 publications receiving 77778 citations. Previous affiliations of Stephen R. Quake include Agency for Science, Technology and Research & Allegheny Health Network.
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Compositions and methods of delivering treatments for latent viral infections
Stephen R. Quake,Jianbin Wang +1 more
TL;DR: In this paper, the authors provide delivery methods and compositions for antiviral therapeutics, such as adenovirus, AAV, and replication incompetent HSV, which can be used as vehicles to deliver DNA vectors encoding a nuclease or a cell-killing gene.
Journal ArticleDOI
65: Digital PCR enables rapid prenatal diagnosis of fetal aneuploidy
PatentDOI
Noninvasive prenatal diagnosis of single-gene disorders using droplet digital pcr
TL;DR: The authors' method detects single nucleotide mutations of autosomal recessive diseases as early as the first trimester of pregnancy, of importance for metabolic disorders where early diagnosis can affect management of the disease and reduce complications and anxiety related to invasive testing.
Functional perfluoropolyethers as novel materials for microfluidics and soft lithography
Jason P. Rolland,R. Michael van Dam,Erik C. Hagberg,Kenneth R. Carter,Stephen R. Quake,Joseph M. DeSimone +5 more
TL;DR: In this article, the authors proposed a method for the synthesis of polymeric interfaces and macromolecular assemblages using the IBM Almaden Research Center at IBM's Silicon Valley Research Center.
Posted ContentDOI
Single-cell profiling identifies ACE+ granuloma macrophages as a nonpermissive niche for intracellular bacteria during persistent Salmonella infection
Trung H.M. Pham,Yu Xue,Susan M. Brewer,Kenneth H. Bernstein,Stephen R. Quake,Denise M. Monack +5 more
TL;DR: It is shown that ACE+ granuloma macrophages have restricted capacity to act as a cellular niche that enables intracellular bacterial persistence, and disruption of pathogen control by neutralizing TNF preferentially depletes ACE+ macrophage in infected tissues.