ERP PACKAGE EVALUATION, THE CASE OF SMEs KAVALA’s REGION

In this paper we want to examine how enterprise resource planning (ERP) systemseffects on small and medium-sized enterprises (SMEs) Kavala’s region. We consider several SMEsof our region, we use data from each SME and we form a questionnaire to secure more data fromthe enterprises. We weight up the factors that affect the choice of ERP. Also, we relate these factorswith basic characteristics of the specific SMEs of our region. Flexibility and functionality are themost important criteria of choosing an ERP system. Surprisingly, the cost is one of the lessimportant criteria. Also, minor effects have criteria such as brand, name and position of the vendor.Finally, we indicate issues for future research.ERP, SMEs, criteria evaluation

The basic chemistry of exercise-induced DNA oxidation:oxidative damage, redox signalling and their interplay

Acute exercise increases reactive oxygen and nitrogen species generation. This phenomenon is associated with two major outcomes: (1) redox signalling and (2) macromolecule damage. Mechanistic knowledge of how exercise-induced redox signalling and macromolecule damage are interlinked is limited. This review focuses on the interplay between exercise-induced redox signalling and DNA damage, using hydroxyl radical (·OH) and hydrogen peroxide (H2O2) as exemplars. It is postulated that the biological fate of H2O2 links the two processes and thus represents a bifurcation point between redox signalling and damage. Indeed, H2O2 can participate in two electron signalling reactions but its diffusion and chemical properties permit DNA oxidation following reaction with transition metals and ·OH generation. It is also considered that the sensing of DNA oxidation by repair proteins constitutes a non-canonical redox signalling mechanism. Further layers of interaction are provided by the redox regulation of DNA repair proteins and their capacity to modulate intracellular H2O2 levels. Overall, exercise-induced redox signalling and DNA damage may be interlinked to a greater extent than was previously thought but this requires further investigation

Editorial: Psychophysiology of Stress

Stress is a multifactorial complex phenomenon where organic resources are mobilized to deal with a real or perceived threat (Cohen et al., 1983). The stress response is one of the most important phylogenetic coping mechanisms that have allowed humans to successfully adapt to highly demanding and potentially dangerous contexts (Hadany et al., 2006; Korzan and Summers, 2021). The intrinsic neurobiological mechanisms involved in the stress response have not changed much in the last stages of the evolution of the human being, prominently including the hypothalamic-pituitary-adrenocortical axis and the autonomic nervous system (Ulrich-Lai and Herman, 2009;McEwen et al., 2015; Cohen et al., 2016). In contrast, our social context has changed dramatically recently in evolutionary terms

Influence of vitamin C and vitamin E on redox signalling:implications for exercise adaptations

The exogenous antioxidants vitamin C (ascorbate) and vitamin E (α-tocopherol) often blunt favourable cell signalling responses to exercise, suggesting that redox signalling contributes to exercise adaptations. Current theories posit that this antioxidant paradigm interferes with redox signalling by attenuating exercise-induced reactive oxygen species (ROS) and reactive nitrogen species (RNS) generation. The well-documented in vitro antioxidant actions of ascorbate and α-tocopherol and characterisation of the type and source of the ROS/RNS produced during exercise theoretically enables identification of the redox-dependent mechanism responsible for the blunting of favourable cell signalling responses to exercise. This review aimed to apply this reasoning to determine how the aforementioned antioxidants might attenuate exercise-induced ROS/RNS production. The principal outcomes of this analysis are (1) neither antioxidant is likely to attenuate nitric oxide signalling either directly (reaction with nitric oxide) or indirectly (reaction with derivatives, e.g. peroxynitrite) (2) neither antioxidant reacts appreciably with hydrogen peroxide, a key effector of redox signalling (3) ascorbate but not α-tocopherol has the capacity to attenuate exercise-induced superoxide generation and (4) alternate mechanisms, namely pro-oxidant side reactions and/or reduction of bioactive oxidised macromolecule adducts, are unlikely to interfere with exercise-induced redox signalling. Out of all the possibilities considered, ascorbate mediated suppression of superoxide generation with attendant implications for hydrogen peroxide signalling is arguably the most cogent explanation for blunting of favourable cell signalling responses to exercise. However, this mechanism is dependent on ascorbate accumulating at sites rich in NADPH oxidases, principal contributors to contraction mediated superoxide generation, and outcompeting nitric oxide and superoxide dismutase isoforms. The major conclusions of this review are: (1) direct evidence for interference of ascorbate and α-tocopherol with exercise-induced ROS/RNS production is lacking (2) theoretical analysis reveals that both antioxidants are unlikely to have a major impact on exercise-induced redox signalling and (3) it is worth considering alternate redox-independent mechanisms