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Mitchell L. Sogin

Researcher at Marine Biological Laboratory

Publications -  233
Citations -  53534

Mitchell L. Sogin is an academic researcher from Marine Biological Laboratory. The author has contributed to research in topics: Ribosomal RNA & Phylogenetic tree. The author has an hindex of 40, co-authored 232 publications receiving 49277 citations. Previous affiliations of Mitchell L. Sogin include Bigelow Laboratory For Ocean Sciences & Woods Hole Oceanographic Institution.

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A core gut microbiome in obese and lean twins

TL;DR: The faecal microbial communities of adult female monozygotic and dizygotic twin pairs concordant for leanness or obesity, and their mothers are characterized to address how host genotype, environmental exposure and host adiposity influence the gut microbiome.
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Microbial diversity in the deep sea and the underexplored “rare biosphere”

TL;DR: It is shown that bacterial communities of deep water masses of the North Atlantic and diffuse flow hydrothermal vents are one to two orders of magnitude more complex than previously reported for any microbial environment.
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Rapid determination of 16S ribosomal RNA sequences for phylogenetic analyses

TL;DR: A protocol is described for rapidly generating large blocks of 16S rRNA sequence data without isolation of the 16 S rRNA or cloning of its gene, and its phylogenetic usefulness is evaluated by examination of several 17S rRNAs whose gene sequences are known.
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The characterization of enzymatically amplified eukaryotic 16S-like rRNA-coding regions.

TL;DR: Oligodeoxynucleotides that are complementary to conserved regions at the 5' and 3' termini of eukaryotic 16S-like rRNAs were used to prime DNA synthesis in repetitive cycles of denaturation, reannealing, and DNA synthesis.
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The Pervasive Effects of an Antibiotic on the Human Gut Microbiota, as Revealed by Deep 16S rRNA Sequencing

TL;DR: Ciprofloxacin treatment influenced the abundance of about a third of the bacterial taxa in the gut, decreasing the taxonomic richness, diversity, and evenness of the community, and support the hypothesis of functional redundancy in the human gut microbiota.