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Kleopatra H. Schulpis

Bio: Kleopatra H. Schulpis is an academic researcher from Boston Children's Hospital. The author has contributed to research in topics: Na+/K+-ATPase & Galactosemia. The author has an hindex of 27, co-authored 166 publications receiving 2516 citations. Previous affiliations of Kleopatra H. Schulpis include Athens State University & National and Kapodistrian University of Athens.


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Journal ArticleDOI
TL;DR: Gal and its derivatives may produce free radicals in the suckling rat brain, reported for first time, and the addition of the above antioxidants may reduce the consequences of brain Mg2+ -ATPase activation by Gal and Galtol in galactokinase deficiency galactosaemia.

134 citations

Journal ArticleDOI
TL;DR: Phe could protect against the direct action of (*)OH radicals on brain AChE and in this way it might be useful in the prevention of certain cholinergic neural dysfunctions.

120 citations

Journal ArticleDOI
TL;DR: It is suggested that the antioxidant action of Cys and GSH may be due to the binding of free radicals to sulfhydryl groups of the molecule, so that free radicals cannot induce Na+,K+-ATPase inhibition.
Abstract: The aim of this study was to investigate whether the preincubation of brain homogenates with L-phenylalanine (Phe), L-cysteine (Cys) or reduced glutathione (GSH) could reverse the free radical effects on Na+,K+-ATPase activity. Two well established systems were used for the production of free radicals: 1) FeSO4 (84 microM) plus ascorbic acid (400 microM) and 2) FeSO4, ascorbic acid and H2O2 (1 mM) for 10 min at 37 degrees C in homogenates of adult rat whole brain. Changes in brain Na+,K+-ATPase activity and total antioxidant status (TAS) were studied in the presence of each system separately, with or without Phe, Cys or GSH. TAS value reflects the amount of free radicals and the capacity of the antioxidant enzymes to limit the free radicals in the homogenate. Na+,K+-ATPase was inhibited by 35-50% and TAS value was decreased by 50-60% by both systems of free radical production. The enzymatic inhibition was completely reversed and TAS value increased by 150-180% when brain homogenates were preincubated with 0.83 mM Cys or GSH. However, this Na+,K+-ATPase inhibition was not affected by 1.80 mM Phe, which produced a 45-50% increase in TAS value. It is suggested that the antioxidant action of Cys and GSH may be due to the binding of free radicals to sulfhydryl groups of the molecule, so that free radicals cannot induce Na+,K+-ATPase inhibition. Moreover, Cys and GSH could regulate towards normal values the neural excitability and metabolic energy production, which may be disturbed by free radical action on Na+,K+-ATPase.

80 citations

Journal ArticleDOI
TL;DR: The aim of this review is to provide an up-to-date synopsis of the available knowledge regarding the aforementioned alterations that take place in the hippocampus due to fetal-, neonatal- or adult-onset hypothyroidism.
Abstract: Thyroid hormones (THs) exert a broad spectrum of effects on the central nervous system (CNS). Hypothyroidism, especially during CNS development, can lead to structural and functional changes (mostly resulting in mental retardation). The hippocampus is considered as one of the most important CNS structures, while the investigation and understanding of its direct and indirect interactions with the THs could provide crucial information on the neurobiological basis of the (frequently-faced in clinical practice) hypothyroidism-induced mental retardation and neurobehavioral dysfunction. THs-deficiency during the fetal and/or the neonatal period produces deleterious effects for neural growth and development (such as reduced synaptic connectivity, delayed myelination, disturbed neuronal migration, deranged axonal projections, decreased synaptogenesis and alterations in neurotransmitters' levels). On the other hand, the adult-onset thyroid dysfunction is usually associated with neurological and behavioural abnormalities. In both cases, genomic and proteomic changes seem to occur. The aim of this review is to provide an up-to-date synopsis of the available knowledge regarding the aforementioned alterations that take place in the hippocampus due to fetal-, neonatal- or adult-onset hypothyroidism.

78 citations

Journal ArticleDOI
TL;DR: It could be suggested that diet changes in the Greek population, especially in children and adolescents, living in big cities is significantly influencing their total cholesterol profiles throughout the last 10 years.
Abstract: Objective To elucidate associations of age and sex with serum cholesterol and triglyceride levels and to provide for the first time percentile distribution data for pediatric lipids Participants and Methods A high sample of 7767 (3980 boys, 3787 girls) fasting schoolchildren, 6 to 14 years of age, were studied in Athens, Greece Results The mean cholesterol ranged from 157 to 174 mg/dL for boys and from 158 to 172 mg/dL for girls peaking at 9 years of age for both sexes Triglyceride levels also tended to increase gradually and to peak at 11 years of age for both sexes The high-density lipoprotein cholesterol levels were highest at 9 years of age for both sexes and the low-density lipoprotein cholesterol levels also tended to peak at 9 years of age for boys and at 8 years of age for girls Atherogenic indices ranged from 154 to 168 for boys and 151 to 185 for girls Conclusion According to these findings, it could be suggested that diet changes in the Greek population, especially in children and adolescents, living in big cities is significantly influencing their total cholesterol profiles throughout the last 10 years

73 citations


Cited by
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TL;DR: In this article, the authors discuss how extrinsic incentives may come into conflict with other motivations and examine the research literature on three important examples in which monetary incentives have been used in a non-employment context to foster the desired behavior: education, increasing contributions to public goods, and helping people change their lifestyles, particularly with regard to smoking and exercise.
Abstract: First we discuss how extrinsic incentives may come into conflict with other motivations. For example, monetary incentives from principals may change how tasks are perceived by agents, with negative effects on behavior. In other cases, incentives might have the desired effects in the short term, but they still weaken intrinsic motivations. To put it in concrete terms, an incentive for a child to learn to read might achieve that goal in the short term, but then be counterproductive as an incentive for students to enjoy reading and seek it out over their lifetimes. Next we examine the research literature on three important examples in which monetary incentives have been used in a nonemployment context to foster the desired behavior: education; increasing contributions to public goods; and helping people change their lifestyles, particularly with regard to smoking and exercise. The conclusion sums up some lessons on when extrinsic incentives are more or less likely to alter such behaviors in the desired directions.

1,460 citations

Journal ArticleDOI
TL;DR: This volume, more than most, explains the contributions of the laboratory to clinical medicine, and shedding light on fundamental metabolic sequences and biologic mechanisms.
Abstract: This book is one of our contemporary medical bibles. It needs no introduction; those who have frequent need of it know it very well, and those who use it less often seek it out on the library shelf when problems arise. The book is truly encyclopedic. Everything relevant discovered during the six-year intervals between publication finds its way into these pages. By today's standards, its 1,778 closely packed small-print pages are a bargain. The mutant gene is both hero and villain in this book. It is reponsible for the biochemical abnormality that results in disease, no matter how rare a given abnormality may be. By the same token, however, it is truly an experiment of nature, shedding light on fundamental metabolic sequences and biologic mechanisms. This volume, more than most, explains the contributions of the laboratory to clinical medicine. Each chapter seems to have been rewritten, so that the exciting

1,117 citations

Journal Article
TL;DR: A defect in an enzyme called glucose-6-phosphate dehydrogenase causes red blood cells to break down prematurely, which results in the destruction ofRed blood cells, which carry oxygen from the lungs to tissues throughout the body.
Abstract: Glucose-6-phosphate dehydrogenase deficiency is a genetic disorder that occurs almost exclusively in males. This condition mainly affects red blood cells, which carry oxygen from the lungs to tissues throughout the body. In affected individuals, a defect in an enzyme called glucose-6-phosphate dehydrogenase causes red blood cells to break down prematurely. This destruction of red blood cells is called hemolysis.

1,006 citations

Journal ArticleDOI
TL;DR: Cutaneous expression of the CRH/POMC system is highly organized, encoding mediators and receptors similar to the hypothalamic-pituitary-adrenal (HPA) axis, that in the skin is expressed as a highly localized response which neutralizes noxious stimuli and attendant immune reactions.
Abstract: The skin is a known target organ for the proopiomelanocortin (POMC)-derived neuropeptides alpha-melanocyte stimulating hormone (alpha-MSH), beta-endorphin, and ACTH and also a source of these peptides. Skin expression levels of the POMC gene and POMC/corticotropin releasing hormone (CRH) peptides are not static but are determined by such factors as the physiological changes associated with hair cycle (highest in anagen phase), ultraviolet radiation (UVR) exposure, immune cytokine release, or the presence of cutaneous pathology. Among the cytokines, the proinflammatory interleukin-1 produces important upregulation of cutaneous levels of POMC mRNA, POMC peptides, and MSH receptors; UVR also stimulates expression of all the components of the CRH/POMC system including expression of the corresponding receptors. Molecular characterization of the cutaneous POMC gene shows mRNA forms similar to those found in the pituitary, which are expressed together with shorter variants. The receptors for POMC peptides expressed in the skin are functional and include MC1, MC5 and mu-opiate, although most predominant are those of the MC1 class recognizing MSH and ACTH. Receptors for CRH are also present in the skin. Because expression of, for example, the MC1 receptor is stimulated in a similar dose-dependent manner by UVR, cytokines, MSH peptides or melanin precursors, actions of the ligand peptides represent a stochastic (predictable) nonspecific response to environmental/endogenous stresses. The powerful effects of POMC peptides and probably CRH on the skin pigmentary, immune, and adnexal systems are consistent with stress-neutralizing activity addressed at maintaining skin integrity to restrict disruptions of internal homeostasis. Hence, cutaneous expression of the CRH/POMC system is highly organized, encoding mediators and receptors similar to the hypothalamic-pituitary-adrenal (HPA) axis. This CRH/POMC skin system appears to generate a function analogous to the HPA axis, that in the skin is expressed as a highly localized response which neutralizes noxious stimuli and attendant immune reactions.

730 citations