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Ration have soared over the past several decades, suggesting that exposures rather than genetics dictate their etiologies. Our over-arching hypothesis is that shifts in lifestyles and economics have led us to chronically consume excess fat, and get exposed to agents that cause insulin resistance. Consideration given to potential pathogenic agents was focused by the experimental evidence showing th
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Ion of immortalized MARCO and SR-AI/II-deficient murine alveolar macrophage cell linesHongwei Zhou1, Amy Imrich1 and Lester Kobzik*1,Address: 1Department of Environmental Health, Harvard School of Public Health, Boston, MA, 02115, USA and 2Department of Pathology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA Email: Hongwei Zhou - hzhou@hsph.harvard.edu; Amy Imrich -
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Urces. Therefore, we entertained the hypothesis that either limited or chronic low-level exposures to nitrosamines account for the observed shifts in morbidity and mortality from insulin resistance diseases. Moreover, given the clear role of high dietary fat intake as a mediator of obesity, T2DM, or cognitive impairment, we proposed that the combined effects of HFD and NDEA exposure may act additi
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Onfim I, Camacho RJ, Vandamme AM, Lemey P: Phylodynamics of the HIV-1 CRF02_AG clade in Cameroon. Infect Genet Evol 2012, 12:453?60. 20. Zhang M, Foley B, Schultz AK, Macke JP, Bulla I, Stanke M, Morgenstern B, Korber B, Leitner T: The role of recombination in the emergence of a complex and dynamic HIV epidemic. Retrovirology 2010, 7:25. 21. Carr JK, Salminen MO, Albert J, Sanders-Buell E, Gotte D
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F HNE were similar in the HFD+VEH and HFD+NDEA groups, and both were significantly higher than in the LFD+VEH and LFD +NDEA groups (P
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