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Minghsun Liu

Researcher at University of California, Los Angeles

Publications -  21
Citations -  2590

Minghsun Liu is an academic researcher from University of California, Los Angeles. The author has contributed to research in topics: Propionibacterium acnes & Gene. The author has an hindex of 16, co-authored 21 publications receiving 2207 citations. Previous affiliations of Minghsun Liu include Stanford University & Massachusetts Institute of Technology.

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Pyrosequencing study of fecal microflora of autistic and control children

TL;DR: If the unique microbial flora is found to be a causative or consequent factor in this type of autism, it may have implications with regard to a specific diagnostic test, its epidemiology, and for treatment and prevention.
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Propionibacterium acnes Strain Populations in the Human Skin Microbiome Associated with Acne

TL;DR: This study demonstrates a previously unreported paradigm of commensal strain populations that could explain the pathogenesis of human diseases and underscores the importance of strain level analysis of the human microbiome to define the role of Commensals in health and disease.
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Reverse transcriptase-mediated tropism switching in Bordetella bacteriophage

TL;DR: A group of temperate bacteriophages that generate diversity in a gene, designatedmtd (major tropism determinant), which specifies tropism for receptor molecules on host Bordetella species is identified.
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Tropism switching in Bordetella bacteriophage defines a family of diversity-generating retroelements

TL;DR: It is proposed that a TR reverse transcript is mutagenized, integrated into VR as a single non-coding strand, and then partially converted to the parental VR sequence, which allows the diversity-generating system to minimize variability to the subset of bases under selection.
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Dissection of the Burkholderia intracellular life cycle using a photothermal nanoblade.

TL;DR: The data suggest that the primary means for intercellular spread involves cell fusion, as opposed to pseudopod engulfment and bacterial escape from double-membrane vacuoles, and that plaque formation represents MNGC death.