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Cer. Clin Cancer Res. 2009;15(17):5308?6. 80. Degterev A, Yuan J. Expansion and evolution of cell death programmes. Nat Rev Mol Cell Biol. 2008;9(5):378?0. 81. Shen HM, Codogno P. Autophagy is a survival force via suppression of necrotic cell death. Exp Cell Res. 2012;318(11):1304?. 82. Munoz-Gamez JA, Rodriguez-Vargas JM, Quiles-Perez R, Aguilar-Quesada R, Martin-Oliva D, de Murcia G, et al. PAR
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 t
N male rats.Parameter Duration of aggression/sec GROUP Control Leaded gasoline Unleaded gasoline Tooth chattering 0.9 ?0.23 4.7 ?1.1 a** 4.4 ?0.92 a* Threat posture 1.5 ?0.54 6 ?1.2 a* 6.2 ?1.31 a* Leaping and biting 1.9 ?0.72 5.5 ?1.45 5.9 ?1.50 Boxing position 1 ?0.42 2.2 ?0.63 2.2 ?0.Values are expressed as means ?SE a: significantly different from the control group. Asterisks indicate the lev
Sible to interpret these results in the light of the effects of gasoline constituents. Another study demonstrated that lead exposure enhances predatory aggression in the cat and provide experimental support for a causal relationship between lead exposure and aggressive behaviour in humans [56]. This was concomitant with deficiency in serotonin that plays an important role to counteract the aggres
Nnervations reaches out to the hypothalamus to regulate secretion of TRH and prolactin secretion, and then projects to the brain limbic system to modulate motivations and emotions [47]. So, gasoline induced impairment of the DA system would result in serious impacts on the neural control of voluntary locomotion and would affect several behavioural aspects.In the present study, the norepinephrine
R protein; AbPP-Ab: amyloid-b peptide; AChE: acetylcholinesterase; AD: Alzheimer's disease; CER: Ceramide synthase; ChAT: choline acetyltransferase; ELISA: enzyme-linked immunosorbant assay; GFAP: glial fibrillary acidic protein; GSK-3b: glycogen synthase kinase-3b; H E: hematoxylin and eosin; HFD: high fat diet; HNE: 4-hydroxy-2-nonenal; HRP: horseradish peroxidase; i.p.: intraperitoneal; IGF: I
Ation and glial cytoplasmic inclusions. Ann Neurol 1996, 39(2):241-255. 49. Burk K, Globas C, Wahl T, Buhring U, Dietz K, Zuhlke C, Luft A, Schulz JB, Voigt K, Dichgans J: MRI-based volumetric differentiation of sporadic cerebellar ataxia. Brain 2004, 127(Pt 1):175-181.50. Dickson DW, Lin W, Liu WK, Yen SH: Multiple system atrophy: a sporadic synucleinopathy. Brain Pathol 1999, 9(4):721-732. 51.
Ation and glial cytoplasmic inclusions. Ann Neurol 1996, 39(2):241-255. 49. Burk K, Globas C, Wahl T, Buhring U, Dietz K, Zuhlke C, Luft A, Schulz JB, Voigt K, Dichgans J: MRI-based volumetric differentiation of sporadic cerebellar ataxia. Brain 2004, 127(Pt 1):175-181.50. Dickson DW, Lin W, Liu WK, Yen SH: Multiple system atrophy: a sporadic synucleinopathy. Brain Pathol 1999, 9(4):721-732. 51.
S performed using the ABC method, and revealed with DAB (brown precipitate)-see Experimental Procedures. Sections were lightly counterstained with Hematoxylin (blue) to help reveal the tissue architecture. Cerebellar layers: ml = molecular layer; pc = Purkinje cell layer; gc = granule cell layer; wm = white matter. Note focal pc loss in A2, and large zones of pc loss in A3 and A4. (Original Magni
Ds, and cholesterol levels compared with LFD+VEH and LFD +NDEA treated groups. In addition, the serum free fatty acid level was significantly lower in the LFD+NDEA compared with LFD+VEH treated rats, whereas the triglyceride and cholesterol levels were similar in the two groups. Therefore, hyperglycemia, hyper-insulinemia, and hyper-leptinemia were features of chronic HFD feeding, and worsened by
N E, Longato L, Jiao P, Mark P, Wands JR, Xu H, de la Monte SM: Hepatic Ceramide May Mediate Brain Insulin Resistance and Neurodegeneration in Type 2 Diabetes and Nonalcoholic Steatohepatitis. J Alzheimers Dis 2009, 16(4):715-729. 46. Moroz N, Tong M, Longato L, Xu H, de la Monte SM: Limited Alzheimertype neurodegeneration in experimental obesity and type 2 diabetes mellitus. J Alzheimers Dis 200
R palsy. J Neuropathol Exp Neurol 2001, 60(5):403-410. 64. Rusina R, Bourdain F, Matej R: [Multiple system atrophy and Alzheimer's disease: a case report of a rare association of two neuro-degenerative disorders]. Rev Neurol (Paris) 2007, 163(12):1239-1241. 65. Engel PA, Grunnet M: Atypical dementia and spastic paraplegia in a patient with primary lateral sclerosis and numerous necortical beta am
R protein; AbPP-Ab: amyloid-b peptide; AChE: acetylcholinesterase; AD: Alzheimer's disease; CER: Ceramide synthase; ChAT: choline acetyltransferase; ELISA: enzyme-linked immunosorbant assay; GFAP: glial fibrillary acidic protein; GSK-3b: glycogen synthase kinase-3b; H E: hematoxylin and eosin; HFD: high fat diet; HNE: 4-hydroxy-2-nonenal; HRP: horseradish peroxidase; i.p.: intraperitoneal; IGF: I
P. Chronic HFD feeding aloneTable 3 Effects of High Fat Diet and NDEA Exposure on Biomarkers of Insulin and IGF Resistance in the CerebellummRNA AbPP Tau AChE ChAT Insulin IGF-1 IGF-2 Insulin R IGF-1R IGF-2R IRS-1 IRS-2 IRS-4 LFD+VEH 7.007 ?0.828 12.230 ?1.098 2.829 ?0.178 0.701 ?0.045 0.754 ?0.048 0.957 ?0.119 12.000 ?1.800 17.090 ?1.547 5.031 ?0.525 5.677 ?0.548 5.559 ?0.411 7.701 ?0.509 0.135

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