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Varna, Bulgaria

Grant
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. Source


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. Source


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. Source


Tonchev A.B.,Medical University-Varna
Archives Italiennes de Biologie | Year: 2011

Generation of new neurons persists in the normal adult mammalian brain, with neural stem/progenitor cells residing in at least two brain regions: the subventricular zone (SVZ) of the lateral ventricle and the subgranular zone (SGZ) of the dentate gyrus (DG). Adult neurogenesis is well documented in the rodent, and has also been demonstrated in vivo in non-human primates and humans. Brain injuries such as ischemia affect neurogenesis in adult rodents as both global and focal ischemic insults enhance the proliferation of progenitor cells residing in SGZ or SVZ. We addressed the issue whether an injury-triggered activation of endogenous neuronal precursors also takes place in the adult primate brain. We found that the ischemic insult increased the number of progenitor cells in monkey SGZ and SVZ, and caused gliogenesis in the ischemia-prone hippocampal CA1 sector. To better understand the mechanisms regulating precursor cell division and differentiation in the primate, we analyzed the expression at protein level of a panel of potential regulatory molecules, including neurotrophic factors and their receptors. We found that a fraction of mitotic progenitors were positive for the neurotrophin receptor TrkB, while immature neurons expressed the neurotrophin receptor TrkA. Astroglia, ependymal cells and blood vessels in SVZ were positive for distinctive sets of ligands/receptors, which we characterized. Thus, a network of neurotrophic signals operating in an autocrine or paracrine manner may regulate neurogenesis in adult primate SVZ. We also analyzed microglial and astroglial proliferation in postischemic hippocampal CA1 sector. We found that proliferating postischemic microglia in adult monkey CA1 sector express the neurotrophin receptor TrkA, while activated astrocytes were labeled for nerve growth factor (NGF), ligand for TrkA, and the tyrosine kinase TrkB, a receptor for brain-derived neurotrophic factor (BDNF). These results implicate NGF and BDNF as regulators of postischemic glial proliferation in adult primate hippocampus. Source

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