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Zachary D. Kurtz

Researcher at New York University

Publications -  17
Citations -  2535

Zachary D. Kurtz is an academic researcher from New York University. The author has contributed to research in topics: Gut flora & Normalization (statistics). The author has an hindex of 12, co-authored 16 publications receiving 1865 citations. Previous affiliations of Zachary D. Kurtz include Stony Brook University.

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Sparse and Compositionally Robust Inference of Microbial Ecological Networks

TL;DR: SParse InversE Covariance Estimation for Ecological Association Inference is presented, a statistical method for the inference of microbial ecological networks from amplicon sequencing datasets that outperforms state-of-the-art methods to recover edges and network properties on synthetic data under a variety of scenarios.
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Helminth infection promotes colonization resistance via type 2 immunity

TL;DR: It is found that helminth infection protects mice deficient in the Crohn’s disease susceptibility gene Nod2 from intestinal abnormalities by inhibiting colonization by an inflammatory Bacteroides species, and this results support a model of the hygiene hypothesis in which certain individuals are genetically susceptible to the consequences of a changing microbial environment.
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Helminth Colonization Is Associated with Increased Diversity of the Gut Microbiota

TL;DR: It is suggested that helminth-colonized individuals had greater species richness and number of observed OTUs with enrichment of Paraprevotellaceae, especially with Trichuris infection.
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Alternatively activated macrophages derived from monocytes and tissue macrophages are phenotypically and functionally distinct

TL;DR: By transcriptional profiling analysis, it is shown that, although both monocyte and tissue-derived AAMs expressed high levels of Arg1, Chi3l3, and Retnla, only monocyte-derivedAAMs up-regulated Raldh2 and PD-L2, and monocytes' properties associated with immune regulation may depend on the distinct lineage of these cells.
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Antibiotic perturbation of the murine gut microbiome enhances the adiposity, insulin resistance, and liver disease associated with high-fat diet.

TL;DR: These studies form the basis for new models of type 2 diabetes and NAFLD that involve microbiome perturbation and showed topological shifts concurrent with growth promotion and suggest the presence of keystone species.