bluuebunny/crossref_metadata_2025_split huggingface dataset:
G72/G30 (DAOA) and juvenile‐onset mood disorders
Authors: Gomez Lissette , Wigg Karen , Feng Yu , Kiss Eniko , Kapornai Krisztina , Tamás Zsuzsa , Mayer László , Baji Ildikó , Daróczi Gabriella , Benák István , Kothencné Viola Osváth , Dombovári Edit , Kaczvinszk Emília , Besnyő Márta , Gádoros Julia , King Nicole , Székely Judit , Kovacs Maria , Vetró Ágnes , Kennedy James L , Barr Cathy L 
Published: December 2008

AbstractThe chromosome 13q region has been linked to bipolar disorder in a number of genome scans as well as focused linkage studies. Previously we identified linkage to the 13q32 region in a genome scan of 146 affected sibling pair families from Hungary with juvenile‐onset mood disorders. Within this region are the overlapping genes G72/G30, with G72 now officially named as D‐amino‐acid oxidase activator (DAOA). This locus has been associated with panic disorder, schizophrenia, and bipolar disorder. In this study, we tested for association to 11 markers in these genes and mood disorders in a sample of 646 nuclear families identified with a proband with onset of a mood disorder before 14.9 years of age. We identified evidence for association to three markers within the gene (rs2391191, rs3918341, rs1935062), two of which had been associated with bipolar disorder in previous studies. When corrected for the number of markers tested, the results were no longer significant, however the prior evidence for association of this gene in multiple studies points to this gene as a potential contributor to juvenile‐onset mood disorders. © 2008 Wiley‐Liss, Inc.
pH‐Controllable Supramolecular Systems
Authors: Leung Ken Cham‐Fai , Chak Chun‐Pong , Lo Chui‐Man , Wong Wing‐Yan , Xuan Shouhu , Cheng Christopher H. K. 
Published: December 2008

AbstractProton, all that matters! This Focus Review surveys representative examples of pH‐controllable supramolecular systems with interesting features and state‐of‐the‐art applications, which can lead to the construction of meaningful molecular machines for electronic and biological applications that can be controlled by simple perturbation with acid and base.magnified imageThis Focus Review surveys representative examples of pH‐controllable supramolecular systems with interesting features and state‐of‐the‐art applications such as 1) conformational changes within individual molecules; 2) folding/unfolding of polymers; 3) simultaneous binding of cations and anions; 4) logic function; 5) ON–OFF switchable colorimetric sensing; 6) translocation of macrocycle‐in‐rotaxane molecules; 7) large‐scale movement within molecules; and 8) regulation of the substrate flow in nanocontainers. In particular, systems will be discussed that involve: pH‐induced conformational changes of a resorcinarene cavitand and a bis(iron porphyrin) complex; pH control in assembly and disassembly of supramolecular systems stabilized with different major noncovalent interactions; pH‐driven movements of interlocked molecules involving rotaxanes, molecular elevators, and molecular muscles; and, finally, multicomponent supramolecular systems immobilized on solid supports as pH‐responsive nanovalves for the controlled release of specific substrates. Recent advances in the understanding of pH‐controllable supramolecular systems have led to the construction of meaningful molecular machines for electronic and biological applications that are amenable to control by simple perturbation with acids and bases.
Coupling and decoupling of unfairness and anger in ultimatum bargaining
Authors: Srivastava Joydeep , Espinoza Francine , Fedorikhin Alexander 
Published: December 2008

AbstractAlthough previous research has demonstrated the importance of emotions in ultimatum bargaining, this research provides a more direct, convergent test of the role of anger in explaining rejections of unfair offers in ultimatum bargaining. First, using appraisal theory of emotions, this research examines the extent to which the cognitive appraisal of unfairness leads to the emotion of anger, which in turn, drives punitive behavior (i.e., rejection of offers). Second, this research explores the possibility of decoupling the emotion of anger from its antecedent appraisal of unfairness in order to attenuate responders' inclination to reject unfair offers. Third, following the current research tradition that goes beyond a valence‐based approach, we differentiate between the negative emotions of anger and sadness and examine whether it is the specific emotion of anger that is relevant to the cognitive appraisal of unfairness or the general negative valence of the emotion. Copyright © 2008 John Wiley & Sons, Ltd.
Effects of plasma lipoproteins on the production of superoxide anion by human polymorphonuclear leukocytes in vitro
Authors: Couderc Rémy , Bonneau Christine , Tissot Michéle , Bailleul Sophie , Roch‐Arveiller Monique , Giroud Jean Paul 
Published: December 2008

AbstractPolymorphonuclear leukocytes (PMN) generate highly reactive oxygen derived free radicals that may cause lipoprotein lipid oxidation and so contribute to the pathogenesis of atherosclerosis. On the other hand it has been shown that lipoproteins can alter cell functions in vitro. We therefore studied the effects of atherogenic lipoproteins, VLDL and LDL, on the production of superoxide anion by human PMN in the presence or absence of formyl‐methionyl‐leucyl‐phenylalanine (fMLP). VLDL and LDL stimulate PMN superoxide production and potentialize PMN stimulation by fMLP. The lipid moiety of the lipoproteins might be mainly involved in these effects. The binding of radio‐labelled fMLP to its specific membrane receptor was significantly enhanced in the presence of VLDL and only slightly in the presence of LDL. The study of the signal transduction suggests that modulation of phospholipase D and A2 activities could be involved in the modification by LDL of PMN response to fMLP.
Breakdown of oxidized proteins as a part of secondary antioxidant defenses in mammalian cells
Authors: Grune T. , Davies K. J. A. 
Published: December 2008

AbstractThe degradation of oxidized proteins is an essential part of antioxidant defenses against free radical attack. Selective degradation of oxidatively damaged proteins allows proteolytic systems to function directly in the removal of useless cellular debris and therefore prevent the accumulation of potentially toxic fragments or large aggregates of cross‐linked proteins.The degradation of oxidized proteins in dividing mammalian cells after hydrogen peroxide treatment has been demonstrated. Cells are able to increase proteolysis rates after treatment with moderate levels of oxidants. The role of proteasome in the removal of oxidized proteins has been demonstrated by treatment of cells with an anti‐sense oligodesoxynucleotide to the proteasome C2 subunit gene. This treatment decreases the proteasome content of the cells and prevents increased proteolysis rates after hydrogen peroxide treatment. Thus proteasome clearly plays a role in the removal of oxidized proteins.As part of antioxidant defenses the proteasome provides a second line of defense against the numerous radicals and oxidants which contact cells during their lifetime. The degradation of oxidatively damaged proteins enables cells to recover from a moderate oxidant attack.
A non‐radioactive and two radioactive assays for selenophosphate synthetase activity
Authors: Liu Song‐Yuan , Stadtman Thressa C. 
Published: December 2008

AbstractSelenophosphate synthetase catalyzes the formation of monoselenophosphate (SePO3−3) from ATP and selenide (reaction 1).

In one assay frequently used, [8‐14C]AMP formation from [8‐14C]ATP is estimated after separation of the nucleotides by thin‐layer chromatography. An alternative non‐radioactive assay in which the AMP product is estimated using AMP deaminase is described. The highly oxygen‐labile selenophosphate product can be estimated in an assay employing [γ‐32P]ATP. The 32P‐labeled selenophosphate is converted to [32P]orthophosphate by treatment with iodine and estimated after removal of residual [32P]ATP on charcoal.
cDNA and deduced polypeptide sequence of a mouse selenoprotein P
Authors: Steinert Peter , Ahrens Marion , Gross Gerhard , Flohé Leopold 
Published: December 2008

AbstractAn 11‐day embryonic Swiss Webster/NIH mouse cDNA library was screened with a partial murine selenoprotein P cDNA probe and a murine selenoprotein‐P‐type cDNAThe accession number of the nucleic acid sequence data for murine selenoprotein P in the EMBL Data Library is X99807.
clone of 2075 bp lenght was obtained. The clone contained a 5′‐leader sequence of 132 bp length, the selenoprotein P coding frame, and 803 base pairs in the 3′ untranslated region. Alignment and RNA folding studies revealed the presence of two well conserved selenocysteine inserting motifs in the 3′ flanking region. The deduced polypeptide sequence comprises 380 residues including ten selenocysteines. Identical amino acid residues in homologous positions are 86%, 71%, and 64% when compared to the previously reported selenoprotein P sequences of rat, man, and cattle, respectively. The comparatively low similarity between the selenoprotein P sequences reported so far leaves open the question whether they belong to the same molecular clade.
Lipoic acid increases de novo synthesis of cellular glutathione by improving cystine utilization
Authors: Han Derick , Handelman Garry , Marcocci Lucia , Sen Chandan K. , Roy Sashwati , Kobuchi Hirotsugu , Tritschler Hans J. , Flohé Leopold , Packer Lester 
Published: December 2008

AbstractLipoic acid (thiotic acid) is being used as a dietary supplement, and as a therapeutic agent, and is reported to have beneficial effects in disorders associated with oxidative stress, but its mechanism of action remains unclear. We present evidence that lipoic acid induces a substantial increase in cellular reduced glutathione in cultured human Jurkat T cells, human erythrocytes, C6 glial cells, NB41A3 neuroblastoma cells, and peripheral blood lymphocytes. The effect depends on metabolic reduction of lipoic acid to dihydrolipoic acid. Dihydrolipoic acid is released into the culture medium where it reduces cystine. Cysteine thus formed is readily taken up by the neutral amino acid transport system and utilized for glutathione synthesis. By this mechanism lipoic acid enables cystine to bypass the χ‐c transport system, which is weakly expressed in lymphocytes and inhibited by glutamate. Thereby lipoic acid enables the key enzyme of glutathione synthesis, γ‐glutamylcysteine synthetase, which is regulated by uptake‐limited cysteine supply, to work at optimum conditions. Flow cytometric analysis of freshly prepared human peripheral blood lymphocytes, using monobromobimane labeling of cellular thiols, reveals that lipoic acid acts mainly to normalize a subpopulation of cells severely compromised in thiol status rather than to increase thiol content beyond physiological levels. Hence lipoic acid may have clinical relevance in restoration of severely glutathione deficient cells.
Evidence for a functional relevance of the selenocysteine residue in mammalian thioredoxin reductase
Authors: Marcocci Lucia , Flohé Leopold , Packer Lester 
Published: December 2008

AbstractHuman thioredoxin reductase was recently shown to contain a TGA encoded selenocysteine residue at the penultimate position of its amino acid chain. Depending on the availability of selenium during biosynthesis, an authentic selenocysteine‐containing or a selenium‐free enzyme truncated at the penultimate position is expected to be formed. Correspondingly, the enzymatic activity should be altered by selenium restriction, if the selenocysteine residue is functionally important. In order to check the catalytic role of the selenocysteine residue, four different human cell lines were grown in selenium deficient media or with adequate selenium supplementation (40 nM sodium selenite) and thioredoxin reductase activity was measured as NADPH‐dependent DTNB reduction or thioredoxin‐mediated insulin reduction. Thioredoxin reductase activities, like glutathione peroxidase activities, were consistently higher in selenium supplemented cells, whereas glutathione reductase activity was not affected by the selenium. The dose‐response was similar for thioredoxin reductase and glutathione peroxidase, but the recovery of glutathione peroxidase activity upon selenium supplementation was faster than with thioredoxin reductase. Also the increase of glutathione peroxidase activities was substantially higher than that of thioredoxin reductase (400–1200% versus a maximum of 250%). These observations clearly indicate a catalytic role of the selenocysteine residue in the thioredoxin reductase, but suggest either the existence of a selenium‐unresponsive isoenzyme or a residual disulfide reductase activity in the selenium‐free truncated protein made under conditions of selenium deficiency.
Prevention of diabetes‐induced abnormal retinal blood flow by treatment with d‐α‐tocopherol
Authors: Kunisaki Makoto , Bursell Sven‐Erik , Umeda Fumio , Nawata Hajime , King George L. 
Published: December 2008

AbstractHyperglycemia in diabetes mellitus has been shown to activate diacylglycerol (DAG)‐protein kinase C (PKC) pathway in the vascular tissues, possibly altering vascular function. We have characterized the effects of vitamin E (d‐α‐tocopherol) on activation of PKC and DAG levels in retinal tissues of diabetic rats, and correlated its effects to retinal hemodynamics using video‐based fluorescein angiography (VFA). Comparing streptozotocin‐induced diabetic rats to controls, membranous PKC specific activities were increased by 71% (p< 0.05). Western blot analysis showed that the membranous PKC βII isoform was significantly increased by 133± 45% (p< 0.05). Intraperitoneal injection of d‐α‐tocopherol (40 mg/kg) every other day prevented the increases in membranous PKC specific activity and PKC β II protein shown by immunoblots. Similar to PKC activities, total DAG levels were increased in the retina and were normalized by d‐α‐tocopherol treatment. Physiologically, abnormalities of retinal blood hemodynamics, as measured using VFA, which previously have been reported to be associated with increases of DAG and PKC levels in the diabetic rats, were prevented by d‐α‐tocopherol treatment in diabetic rats. The direct effect of d‐α‐tocopherol on total DAG and [3H]‐palmitate incorporation into DAG were also examined using cultured bovine retinal endothelial cells (REC). Exposure of REC to 22 mM glucose for three days increased total DAG and [3H]‐palmitate labeled DAG levels by 35± 8% and 50± 8%, respectively (p< 0.05). The presence of d‐α‐tocopherol (50 μg/ml) prevented the increase of both total DAG and [3H]‐palmitate labeled DAG levels in cells exposed to 22 mM glucose.These findings suggested that the mechanism of the d‐α‐tocopherol's effect appears to be mediated by the normalization of the hyperglycemia‐induced activation of the DAG‐PKC pathway which leads to the normalization of abnormal retinal blood flow seen in diabetes mellitus.
The role of vitamin E in T‐cell differentiation and the decrease of cellular immunity with aging
Authors: Moriguchi Satoru 
Published: December 2008

AbstractThe purpose of this study is to investigate the effects of vitamin E on both the decrease of cellular immunity with aging (Section 2) and the differentiation of T‐cells in thymus (Section 3). In Section 2, spontaneously hypertensive rats (SHR) as a model for aging were used in this experiment and fed regular (50 IU/kg diet) or a high vitamin E (500 IU/kg diet) diet for 6 weeks. At 12 weeks old, they were killed and assayed. Although proliferation of thymic lymphocytes was significantly decreased in SHR fed the regular diet compared to that of Wistar Kyoto rats (WKY) fed the same diet, the high vitamin E diet induced higher proliferation of thymic lymphocytes in SHR, which was almost the same as that of WKY fed the regular diet. In addition, the expressions of both CD4 and CD8 antigens on CD4+CD8+ T‐cells were also decreased in SHR, which was significantly improved by a high vitamin E diet. These results suggest that a high vitamin E diet enhances thymic lymphocyte proliferation through increased T‐cell differentiation in the thymus. Then, the effect of vitamin E on T‐cell differentiation in the thymus was investigated by using male Fisher rats. Rats were divided into three groups; vitamin E‐free, regular and high vitamin E groups and fed a diet containing various levels of vitamin E (0, 50 and 500 IU/kg diet) for 7 weeks. Although the proportions of CD4+CD8‐ and CD4‐CD8+ T‐cells in thymocytes were significantly greater in the high vitamin E group, the proportion of CD4+CD88‐ T‐cells inversely decreased in the vitamin E‐free group compared to that of the regular group. We have tried to investigate the mechanism on the increased T‐cell differentiation in the thymus of rats fed the high vitamin E diet through cytokine production, thymic epithelial cell (TEC) and macrophage functions. As their results, we have found that vitamin E enhances T‐cell differentiation through the increase of not macrophage but TEC function in the thymus, which is associated with the increased binding capacity of TEC to immature T‐cells via increased expression of the adhesion molecule, ICAM‐1. These results suggest that vitamin E is a potent nutrient for promoting health in the aged via the improvement of cellular immunity decreased with aging.
Can antioxidant supplementation slow the aging process?
Authors: Yu Byung P. , Kang Chang‐Mo , Han Jung‐Soon , Kim Dong Soo 
Published: December 2008

AbstractThe oxidative stress theory of aging is well supported by accumulated evidence from various aging intervention studies. Early antioxidant supplementation studies indicate life span extensions by antioxidant feeding in various experimental organisms. Data collected under tightly controlled conditions show that the feeding of 2‐mercaptoethanol (0.25%) effectively prolonged both the median and maximum life spans of mice. Evidence has been obtained showing dietary vitamin E to protect against oxidative damage to DNA in human lymphocytes and white blood cells. Other clear evidence of vitamin E's protective effect has been seen in its suppressive action of LDL oxidation both in vitro and in vivo. New evidence on the physiological roles of antioxidants, in addition to their well‐known role as free radical scavengers, is emerging from recent research. For instance, the beneficial effect of vitamin E in improving glucose transport and the insulin sensitivity and its putative role as a regulator of cell proliferation should open new research dimensions. This presentation will review some of the anti‐aging aspects of dietary antioxidant supplementation, as well as the potential problems of its long‐term administration that stem from our lack of knowledge about free radical metabolism and the regulation of endogenous defense mechanisms.
Vitamins E plus C and interacting conutrients required for optimal health
Authors: Fred Gey K. 
Published: December 2008

AbstractAntioxidants are crucial components of fruit/vegetable‐rich diets preventing cardiovascular disease (CVD) and cancer:—plasma vitamins C, E, carotenoids from diet correlate prevalence of CVD and cancer inversely, low levels predict an increased risk of individuals which is potentiated by combined inadequacy (e.g., vitamins C+E, C+carotene, A+carotene);—self‐prescribed rectification of vitamins C and E at adequacy of other micronutrients reduce forthcoming CVD, of vitamins A, C, E, carotene and conutrients also cancer;—randomized exclusive supplementation of β‐carotene±vitamin A or E lack benefits except prostate cancer reduction by vitamin E, and overall cancer reduction by selenium;—randomized intervention with synchronous rectification of vitamins A+C+E+B+minerals reduces CVD and counteracts precancerous lesions;—high vitamin E supplements reveal potentials in secondary CVD prevention.Plasma values desirable for primary prevention: ≥30μmol/l lipid‐standardized vitamin E (α‐tocopherol/cholesterol ≥5.0μmol/mmol); ≥50μmol/l vitamin C aiming at vitamin C/vitamin E ratio >1.3–1.5; ≥0.4μmol/l β‐ (≥0.5μmol/l α+β‐) carotene.Conclusions:—in CVD vitamin E acts as first risk discriminator, vitamin C as second one;—optimal health requires synchronously optimized vitamins C+E, A, carotenoids and vegetable conutrients.
Knockout of cellular glutathione peroxidase affects selenium‐dependent parameters similarly in mice fed adequate and excessive dietary selenium
Authors: Cheng Wen‐Hsing , Combs Gerald F. , Lei Xin Gen 
Published: December 2008

AbstractThis study was to determine whether or not effects of the cellular glutathione peroxidase (GPX1) knockout on several Se‐dependent parameters in mice were tissue, dietary Se concentration, and selenoprotein specific. A 2×3 factorial experiment was conducted with 18 GPX1 knockout mice [GPX1(‐)] and 18 controls (3 weeks old, half males and females). These mice were fed a torula yeast diet supplemented with all‐rac‐α‐tocopheryl acetate (50 mg/kg of feed) and Se (sodium selenite) at 0, 0.5, or 3.0 mg/kg of feed for 6 weeks. Both kidney GPX1 mRNA levels and liver, kidney, lung, and testis total GPX activities, assayed using hydrogen peroxide, were affected (p< 0.001) by the GPX1 knockout and dietary Se concentrations, whereas kidney extracellular or plasma GPX (GPX3) mRNA levels and phospholipid hydroperoxide GPX (GPX4) activities in the four tissues were affected (p< 0.001) by only dietary Se concentrations. Total GPX activity in testis was reduced approximately 90% (p< 0.01) by the GPX1 knockout. Neither the GPX1 knockout nor the dietary Se concentrations affected mRNA levels of GPX4 in testis or selenoprotein P in kidney. Total liver Se concentrations were not different between the GPX1(‐) and control mice at 0 mg Se/kg of feed, but were reduced (p< 0.01) by 61 and 64% in the GPX1(‐) mice at 0.5 and 3.0 mg Se/kg of feed, respectively. These results not only confirm the independent expression of GPX3, GPX4, and selenoprotein P from that of GPX1, but also show similar effects of the GPX1 knockout on Se‐dependent parameters in mice between different dietary Se concentrations, tissues, and selenoproteins.
Mitogenic effects of EGF/TGFα and immunolocalization of cognate receptors in human fetal kidneys
Authors: Chailler Pierre , Briáre Normand 
Published: December 2008

AbstractThe involvement of epidermal growth factor (EGF) and homologous transforming growth factor (TGF) in human kidney development was studied by analyzing their effects on the regulation of DNA synthesis in organ culture and by localizing their cognate receptors. Both peptides significantly increased 3H‐thymidine incorporation when added at 10–100 ng/ml, but not at 1–5 ng/ml. Furthermore, addition of an anti‐EGF receptor antibody not only reduced the effect of exogenous EGF (100 ng/ml) on DNA synthesis but decreased basal 3H‐thymidine incorporation. These results indicate that EGF/TGFα are both mitogenic in vitro and further suggest that human fetal kidneys release an endogenous EGF‐related substance masking the effects of low amounts of growth factors added to culture medium. Radioautographic analyses show that EGF (100 ng/ml) increased DNA synthesis in poorly‐differentiated cells of the nephrogenic zone, particularly in subcapsular mesenchyme and peritubular cells; although less responsive, epithelial cells in early nephric tubules represented another target of EGF action. The pattern of EGF/TGFα receptor expression was revealed immunohistochemically at different gestational ages and was shown to be related to the proliferation status. It was maximal in condensing nephrogenic cells, relatively high in newly‐induced epithelium and cortical branches of ureteric epithelium, low in differentiating nephronic cells and nearly absent from renal stroma and medullary collecting ducts. Together, our results indicate that the EGF/TGFα system is directly involved in the regulation of nephrogenic cell proliferation during human metanephrogenesis and it is progressively down‐regulated after conversion of mesenchyme into epithelium.