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Pauline K. Lund

Researcher at University of North Carolina at Chapel Hill

Publications -  64
Citations -  4049

Pauline K. Lund is an academic researcher from University of North Carolina at Chapel Hill. The author has contributed to research in topics: Insulin-like growth factor & In situ hybridization. The author has an hindex of 31, co-authored 64 publications receiving 3855 citations. Previous affiliations of Pauline K. Lund include Johns Hopkins University.

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High-Fat Diet: Bacteria Interactions Promote Intestinal Inflammation Which Precedes and Correlates with Obesity and Insulin Resistance in Mouse

TL;DR: Bacteria and HF diet interact to promote proinflammatory changes in the small intestine, which precede weight gain and obesity and show strong and significant associations with progression of obesity and development of insulin resistance.
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Somatomedin-C/insulin-like growth factor-I and insulin-like growth factor-II mRNAs in rat fetal and adult tissues.

TL;DR: In this article, 32P-labeled complementary DNA probes encoding human and mouse Sm-C/IGF-I and human IGF-II were used in Northern blot hybridization to analyse rat SmC/I and insulin-like growth factor II mRNAs in poly(A+) RNAs from intestine, liver, lung, and brain of adults and fetal rats between day 14 and 17 of gestation.
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Nucleotide sequence analysis of a cDNA encoding human ubiquitin reveals that ubiquitin is synthesized as a precursor.

TL;DR: The finding that Ubiquitin is synthesized as a precursor raises the possibility that the precursor sequence may be important in compartmentalization of ubiquitin or ubiquitIn precursors.
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Growth hormone dependence of somatomedin-C/insulin-like growth factor-I and insulin-like growth factor-II messenger ribonucleic acids.

TL;DR: To investigate the effect of GH status on abundance of Sm-C/IGF-I and IGF-II mRNAs in rat brain, a second experiment was performed that differed from the first in that hypophysectomized rats were given an injection of hGH into the lateral ventricle (intracerebroventricular injection).
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Suppressor of cytokine signaling 3 (SOCS3) limits damage-induced crypt hyper-proliferation and inflammation-associated tumorigenesis in the colon.

TL;DR: It is concluded that cytokine induction of SOCS3 normally provides an intrinsic mechanism to limit injury-induced crypt hyperproliferation and inflammation-associated colon cancer by regulating both STAT3 and NF-κB pathways.