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Quality assessment of milk which is a comprehensive source of nutrients for humans and an important raw material for other dairy products is required in the dairy industry. Rapid, cost-effective, and non-destructive spectroscopic techniques are more preferable than classic wet chemistry approaches for milk analysis. The objective of this work was to review the prediction of milk composition including macronutrients such as fat, protein and lactose and micronutrients such as fatty acids and vitamins using multivariate chemometric modelling of Near Infrared (NIR), Mid Infrared (MIR), fluorescence, and Raman spectral data and data fusion approaches. Literature sources describing spectroscopic analysis of milk samples and the application of multivariate data analysis methods are outlined in this literature review. In addition, the importance of data fusion strategies employed for combing different spectroscopic techniques are reviewed to evaluate their potential to improve the accuracy of the prediction models developed. Recent research studies have demonstrated that the use of data fusion strategies improves the performance of milk composition prediction models developed. [ABSTRACT FROM AUTHOR]

Aims Short-chain acyl-CoA dehydrogenase (SCAD) is a key enzyme in fatty acid oxidation. In the present study we aim to investigate the changes in SCAD between pathological and physiological cardiomyocyte hypertrophy. We also explore the different signaling pathways of pathological and physiological cardiomyocyte hypertrophy. Main methods After neonatal rat cardiomyocytes were treated as setups, cell surface area, expression of SCAD, PPARα, phospho-ERK1/2, activity of SCAD, free fatty acid content and ATP content in the cardiomyocytes were measured. Key findings Neonatal rat cardiomyocytes treated by PE showed an increased cell surface area and free fatty acid content, increased ERK1/2 phosphorylation, decreased expression of PPARα, decreased expression and activity of SCAD and decreased levels of ATP. Neonatal rat cardiomyocytes treated by IGF-1 showed the reverse effects except for the cell surface area. PPARα inhibitor GW6471 and PPARα activator Fenofibrate treatments abrogated the effects induced by IGF-1 and PE in cardiomyocytes respectively, as well as ERK1/2 activator EGF and ERK1/2 inhibitor PD98059. Significance SCAD has different changes between pathological and physiological cardiomyocyte hypertrophy. The ERK1/2/PPARα/SCAD signaling pathways play different roles in pathological and physiological cardiomyocyte hypertrophy. SCAD may be used as a new target to prevent the development of pathological cardiac hypertrophy. [ABSTRACT FROM AUTHOR]

Highlights: [•] Fenofibrate ameliorates cardiac hypertrophy in vivo and in vitro. [•] The interaction between p65-NFκB and NFATc4 regulates cardiac hypertrophy. [•] Fenofibrate attenuates cardiac hypertrophy via activating PPAR-α and thereby preventing the association of p65-NFκB with NFATc4. [Copyright &y& Elsevier]