Sucrose in the concentrated solution or the supercooled “state” : a review of caramelisation reactions and physical behaviour

Sucrose is probably one of the most studied molecules by food scientists, since it plays an important role as an ingredient or preserving agent in many formulations and technological processes. When sucrose is present in a product with a concentration near or greater than the saturation point—i.e. in the supercooled state—it possesses high potentialities for the food industry in areas as different as pastry industry, dairy and frozen desserts or films and coatings production. This paper presents a review on critical issues and research on highly concentrated sucrose solutions—mainly, on sucrose thermal degradation and relaxation behaviour in such solutions. The reviewed works allow identifying several issues with great potential for contributing to significant advances in Food Science and Technology.Authors are grateful for the valuable discussions with Teresa S. Brandao and Rosiane Lopes da Cunha during this research. Author M. A. C. Quintas acknowledges the financial support of her research by FCT grant SFRH/BPD/41715/2007

Epidemiology of cardiac syndrome X and microvascular angina

Chest pain and normal coronary angiography is seen in up 30 % of patients undergoing the investigation. Despite its notable prevalence, the epidemiology of the condition remains poorly documented. Since the turn of the twentieth century, researchers have been baffled by “unmistakable” angina in the absence of coronary artery disease. Curiosity as to the cardiac aetiology of this chest pain became the focus of several key studies investigating the clinical and haemodynamic features of patients with normal coronary angiography. From these early findings, the cardinal features of three specific disorders associated with normal coronary angiography were established – Cardiac Syndrome X, Microvascular Angina and more recently, the Coronary Slow Flow Phenomenon. Although ambiguity in the literature exists, it is likely that an ‘ischemic’ mechanism for the chest pain in these patients is explained by coronary microvascular dysfunction. It also now understood that despite the absence of significant coronary artery disease, the outcomes of patients are not entirely favourable, with studies suggesting a frequent persistence of chest pain, and increased risk of cardiac events, particularly among women. This chapter will review the available epidemiological data on patients with chest pain and normal coronary angiography, and the clinical features and possible aetiological explanations for the specific coronary microvascular disorders.Rosanna Tavella and Guy D. Eslic

Amyloid-β-independent regulators of tau pathology in Alzheimer disease

The global epidemic of Alzheimer disease (AD) is worsening, and no approved treatment can revert or arrest progression of this disease. AD pathology is characterized by the accumulation of amyloid-β (Aβ) plaques and tau neurofibrillary tangles in the brain. Genetic data, as well as autopsy and neuroimaging studies in patients with AD, indicate that Aβ plaque deposition precedes cortical tau pathology. Because Aβ accumulation has been considered the initial insult that drives both the accumulation of tau pathology and tau-mediated neurodegeneration in AD, the development of AD therapeutics has focused mostly on removing Aβ from the brain. However, striking preclinical evidence from AD mouse models and patient-derived human induced pluripotent stem cell models indicates that tau pathology can progress independently of Aβ accumulation and arises downstream of genetic risk factors for AD and aberrant metabolic pathways. This Review outlines novel insights from preclinical research that implicate apolipoprotein E, the endocytic system, cholesterol metabolism and microglial activation as Aβ-independent regulators of tau pathology. These factors are discussed in the context of emerging findings from clinical pathology, functional neuroimaging and other approaches in humans. Finally, we discuss the implications of these new insights for current Aβ-targeted strategies and highlight the emergence of novel therapeutic strategies that target processes upstream of both Aβ and tau