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Background: In prostate adenocarcinoma, the dissection of the expression behaviour of the eukaryotic elongation factors (eEF1A1/2) has not yet fully elucidated.Methods: The EEF1A1/A2 expressions were investigated by real-time PCR, western blotting (cytoplasmic and cytoskeletal/nuclear-enriched fractions) and immunofluorescence in the androgen-responsive LNCaP and the non-responsive DU-145 and PC-3 cells, displaying a low, moderate and high aggressive phenotype, respectively. Targeted experiments were also conducted in the androgen-responsive 22Rv1, a cell line marking the progression towards androgen-refractory tumour. The non-tumourigenic prostate PZHPV-7 cell line was the control.Results: Compared with PZHPV-7, cancer cells showed no major variations in EEF1A1 mRNA; eEF1A1 protein increased only in cytoskeletal/nuclear fraction. On the contrary, a significant rise of EEF1A2 mRNA and protein were found, with the highest levels detected in LNCaP. Eukaryotic elongation factor 1A2 immunostaining confirmed the western blotting results. Pilot evaluation in archive prostate tissues showed the presence of EEF1A2 mRNA in near all neoplastic and perineoplastic but not in normal samples or in benign adenoma; in contrast, EEF1A1 mRNA was everywhere detectable.Conclusion: Eukaryotic elongation factor 1A2 switch-on, observed in cultured tumour prostate cells and in human prostate tumour samples, may represent a feature of prostate cancer; in contrast, a minor involvement is assigned to EEF1A1. These observations suggest to consider EEF1A2 as a marker for prostate cell transformation and/or possibly as a hallmark of cancer progression. [ABSTRACT FROM AUTHOR]

The article reports on the diversity of the patterns of arteries developing atherosclerosis in hypertensive patients. The lesions develop in regions where the flow is either low or turbulent. The marked phenotypic variation between endothelial cells in the different vascular locations, and the different responses of the vascular layers can make a difference in the possibility of the development of atherosclerosis.

Comments on the regulation of energy pressure by a complex network of peptide hormones. Integration of peripheral stimuli and determining behavioral changes related to energy expenditure and food intake; Generation of soluble leptin receptor by alternative splicing of OB-messenger RNA and or ectodomain shedding of membrane-spanning receptors; Capacity of leptin to stimulate fatty-acid oxidation by activating adenylic acid-kinase-activated protein kinase.