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Ed, suggestive of increased myelin degeneration, in these two groups. Ubiquitin immunoreactivity was virtually undetectable in control and NDEA-exposed cerebella (Figs. 1-D1, 1-D2), but slightly increased in the Purkinje and granule cell layers of HFD-fed cerebella (Fig. 1-D3). Rats exposed to NDEA, and also chronically fed with the HFD, had prominently increased ubiquitin immunoreactivity in Purk
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Lusions: Early limited exposure to nitrosamines exacerbates the adverse effects of later chronic high dietary fat intake in promoting T2DM and neurodegeneration. The mechanism involves increased generation of ceramides and probably other toxic lipids in brain.Background The prevalence rates of Alzheimer's Disease (AD), Parkinson's disease (PD), obesity, type 2 diabetes mellitus (T2DM), and metabol
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Fects is clearly warranted. In this regard, guidance may be obtained from what is already known about STZ-induced diseases. STZ, like other N-nitroso compounds, causes cellular injury and disease by functioning as: 1) an alkylating agent and potent mutagen [14]; 2) an inducer of DNA adducts leading to increased apoptosis [23]; 3) a mediator of unscheduled DNA synthesis, triggering cell death [14];
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In HeLa cells. Autophagy. 2011;7(1):27?9. 64. Debnath J, Mills KR, Collins NL, Reginato MJ, Muthuswamy SK, Brugge JS. The role of apoptosis in creating and maintaining luminal space within normal and oncogene-expressing mammary acini. Cell. 2002;111(1):29?0. 65. Fung C, Lock R, Gao S, Salas E, Debnath J. Induction of autophagy during extracellular matrix detachment promotes cell survival. Mol Biol
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Fects is clearly warranted. In this regard, guidance may be obtained from what is already known about STZ-induced diseases. STZ, like other N-nitroso compounds, causes cellular injury and disease by functioning as: 1) an alkylating agent and potent mutagen [14]; 2) an inducer of DNA adducts leading to increased apoptosis [23]; 3) a mediator of unscheduled DNA synthesis, triggering cell death [14];
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Ysiol Cell Physiol. 2012;302(2):C383?91. 68. Sachdev U, Cui X, Hong G, Namkoong S, Karlsson JM, Baty CJ, et al. High mobility group box 1 promotes endothelial cell angiogenic behavior in vitro and improves muscle perfusion in vivo in response to ischemic injury. J Vasc Surg. 2012;55(1):180?1.Yang et al. Cell Bioscience (2015) 5:Page 10 of69. Kang R, Livesey KM, Zeh HJ, Loze MT, Tang D. HMGB1: a
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Ysiol Cell Physiol. 2012;302(2):C383?91. 68. Sachdev U, Cui X, Hong G, Namkoong S, Karlsson JM, Baty CJ, et al. High mobility group box 1 promotes endothelial cell angiogenic behavior in vitro and improves muscle perfusion in vivo in response to ischemic injury. J Vasc Surg. 2012;55(1):180?1.Yang et al. Cell Bioscience (2015) 5:Page 10 of69. Kang R, Livesey KM, Zeh HJ, Loze MT, Tang D. HMGB1: a
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N exist inTable 2 High Fat Diet Feeding and NDEA Treatment Cause Type 2 Diabetes MellitusAssay Body Wt (g) Glucose (mg/dL) Insulin (ng/ml) Leptin Adiponectin Triglyceride (mg/ml) Free Fatty Acids (mM/mg prot) Cholesterol (mg/ml) LFD+VEH 265.100 ?14.050 111.5 ?1.66 0.0611 ?0.017 4.649 ?0.789 20864 ?1454 0.399 ?0.028 0.150 ?0.003 0.943 ?0.024 LFD+NDEA 266.600 ?19.970 128.8* ?4.31 0.163* ?0.038 4.775