Agency: Cordis | Branch: FP7 | Program: CP-FP | Phase: KBBE-2009-2-1-03 | Award Amount: 3.91M | Year: 2010
Objective The ToyBox proposal addresses KBBE-2009-2-1-03 - Behavioural models for prevention of obesity, with a particular focus on children. It will primary aim to influence childrens behaviours and prevent obesity in early childhood. Strategy The proposal will identify key behaviours related to early childhood obesity and their determinants and evaluate behavioural models and educational strategies. Based on the obtained insights at a local level, a multidisciplinary team will develop and implement a school based family involved intervention programme that could be applied on a European scale. Process, impact, outcome and cost-effectiveness evaluation will be conducted to support decision making for European Public Health Policy. Methods The combined use of Precede-Proceed Model and Intervention Mapping will provide the framework for the development, implementation and evaluation of the ToyBox intervention. To achieve this, the project will be subdivided into 10 WPs. This carefully planned stepwise approach will include systematic reviews, secondary analyses of existing data sets, focus group research and school policies overview. Consortium The ToyBox project consortium spans the necessary multidisciplinary variety of experts such as public health experts, epidemiologists, nutritionists, physical activity experts, pedagogists, psychologists, behavioural scientists, nutritionists, paediatricians, early childhood psychologists, health economists, totalling 15 partners, from 10 countries. The consortium, consists of 11 universities, 1 research institute, 2 advocacy groups and an SME representing all regions of Europe. The consortium has ample experience in conducting and coordinating multi-centre international research as well as undertaking dissemination activities to all relevant stakeholders.
Agency: Cordis | Branch: FP7 | Program: CP-IP | Phase: KBBE.2011.2.2-02 | Award Amount: 7.84M | Year: 2012
NutriTech will build on the foundations of traditional human nutrition research using cutting-edge analytical technologies and methods to comprehensively evaluate the diet-health relationship and critically assess their usefulness for the future of nutrition research and human well-being. Technologies include genomics, transcriptomics, proteomics, metabolomics, laser scanning cytometry, NMR based lipoprotein profiling and advanced imaging by MRI/MRS. All methods will be applied in an integrated manner to quantify the effect of diet on phenotypic flexibility, based on metabolic flexibility (the capacity for the organism to adapt fuel oxidation to fuel availability). However, NutriTech will move beyond the state-of-the-art by applying these integrated methods to assess the underlying and related cell biological and genetic mechanisms and multiple physiological processes of adaptation when homeostasis is challenged. Methods will in the first instance be evaluated within a human intervention study, and the resulting optimal methods will be validated in a number of existing cohorts against established endpoints. NutriTech will disseminate the harmonised and integrated technologies on a global scale by a large academic network including 6 non-EU partners and by providing an integrated and standardised data storage and evaluation platform. The impact of NutriTech will be multifold and exploitation is crucial as major breakthroughs from our technology and research are expected. This will be achieved by collaboration with a consortium of 8 major food industries and by exploitation of specific technologies by our 6 SME partners. Overall, NutriTech will lay the foundations for successful integration of emerging technologies intro nutrition research.
Ivanova D.G.,Medical University-Varna
Folia medica | Year: 2013
This overview is an attempt to throw a fresh look at the popular free radical theory of aging (referred to also as oxidative stress theory) which holds that the progressive decline in physiological functions is a result of accumulation of diverse deleterious changes caused by reactive oxygen species (ROS). We discuss the role of mitochondria as a major source of ROS in the cell and how these link accumulation of oxidative damage to the age-related changes in physiologic functions. The free radical theory of aging is analysed here from two different views of aging--one (the pessimistic view) that regards aging as the inevitable result of life activity the consequences of which are accumulation of errors in the genome and damage of the biomolecules, and the other (the optimistic view) which considers that it is the changes in mitochondrial pathways of apoptosis with age that cause the functional tissue changes and aging. We also discuss the possibility of delaying the aging process by appropriate diet or drug therapy, which includes also calorie restriction as a mechanism of modifying the generation of free radicals and body metabolism and thus extending lifespan as a result.
Stettler N.,Childrens Hospital of Philadelphia |
Iotova V.,Medical University-Varna
Current Opinion in Clinical Nutrition and Metabolic Care | Year: 2010
Purpose of review: This review is an update on Recent findings: regarding early growth patterns and later obesity. These data are important because the potential programming of obesity in early life provides hope for new prevention strategies targeting early growth for long-term benefits. Recent findings: Recent findings: regarding the association of childhood or adulthood obesity with fetal growth, gestational weight gain, maternal diabetes, or infancy weight gain are reviewed. Some related outcomes and potential mechanisms are also described. Most studies remain observational and confirm previous findings, but some intervention studies have begun to appear in the recent literature and support some, but not other, observed associations. Summary: Past and Recent findings: confirm the association of early growth patterns with obesity. However, causality must be demonstrated and safety must be established before translating these findings into public health recommendations. © 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins.
Chaldakov G.N.,Medical University-Varna
Archives Italiennes de Biologie | Year: 2011
The field of neurotrophins, particularly, nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF), has witnessed a number of breakthroughs in recent years. There is evidence now that NGF and BDNF mediate multiple biological phenomena, ranging from the Rita Levi-Montalcini's neurotrophic through immunotrophic to epitheliotrophic and nociceptive effects. In 2003 we have enriched the "NGF-ome" with one more expression presented in our concept of NGF metabotrophicity, also that of BDNF. This envisages that these two factors may operate as metabotrophins, that is, involved in the maintenance of cardiometabolic homeostasis (glucose and lipid metabolism as well as energy balance, cardioprotection, and wound healing). Recent results also demonstrated that the circulating and/or tissue levels of NGF and BDNF are altered in cardiometabolic diseases (atherosclerosis, obesity, type 2 diabetes, metabolic syndrome, and type 3 diabetes). Altogether, a hypothesis of metabotrophic deficit due to the reduction of NGF/BDNF availability and/or utilization was raised, and implicated in the pathogenesis of cardiometabolic diseases. This may cultivate a novel pathogenic and therapeutic thinking for these diseases.