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  • 1
    Keywords: brain ; EXPRESSION ; Germany ; DEATH ; PROTEIN ; METABOLISM ; MICE ; DNA ; MECHANISM ; animals ; mechanisms ; fibroblasts ; DISORDER ; ALZHEIMERS-DISEASE ; GLUTATHIONE ; PLASMA ; MUTATION ; REPAIR ; RATES ; PATHOGENESIS ; DIET ; DEMENTIA ; BEHAVIOR ; ANTIOXIDANT ; MEMORY IMPAIRMENT ; DENTATE GYRUS ; STROKE ; DEFICIENCY ; DISORDERS ; ADULT ; review ; fibroblast ; MICE LACKING ; NEURONS ; neurogenesis ; LEVEL ; NUCLEAR ; INDUCE ; GENOTYPE ; PSYCHIATRIC-DISORDERS ; USA ; HOMOCYSTEINE ; depression ; neurodegeneration ; animal ; DEGENERATION ; base excision repair ; DYSFUNCTION ; ADULT HIPPOCAMPAL NEUROGENESIS ; despair ; folate deficiency ; FOLIC-ACID DEFICIENCY ; MAJOR DEPRESSIVE DISORDER ; MILD CEREBRAL-ISCHEMIA ; MITOCHONDRIAL-DNA ; NEURAL-TUBE DEFECTS ; NEURONAL CELL-DEATH ; OXYGEN SPECIES PRODUCTION ; PLASMA HOMOCYSTEINE LEVELS
    Abstract: Folate deficiency and resultant increased homocysteine levels have been linked experimentally and epidemiologically with neurodegenerative conditions like stroke and dementia. Moreover, folate deficiency has been implicated in the pathogenesis of psychiatric disorders, most notably depression. We hypothesized that the pathogenic mechanisms include uracil misincorporation and, therefore, analyzed the effects of folate deficiency in mice lacking uracil DNA glycosylase (Ung(-/-)) versus wild-type controls. Folate depletion increased nuclear mutation rates in Ung(-/-) embryonic fibroblasts, and conferred death of cultured Ung(-/-) hippocampal neurons. Feeding animals a folate-deficient diet (FD) for 3 months induced degeneration of CA3 pyramidal neurons in Ung(-/-) but not Ung(-/-) mice along with decreased hippocampal expression of brain-derived neurotrophic factor protein and decreased brain levels of antioxidant glutathione. Furthermore, FD induced cognitive deficits and mood alterations such as anxious and despair-like behaviors that were aggravated in Ung(-/-) mice. Independent of Ung genotype, FD increased plasma homocysteine levels, altered brain monoamine metabolism, and inhibited adult hippocampal neurogenesis. These results indicate that impaired uracil repair is involved in neurodegeneration and neuropsychiatric dysfunction induced by experimental folate deficiency
    Type of Publication: Journal article published
    PubMed ID: 18614692
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  • 2
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    German Medical Science; Düsseldorf, Köln
    In:  Hypertonie 2004; 28. Wissenschaftlicher Kongress der Deutschen Hochdruckliga; 20041124-20041127; Hannover; DOC04hochP14 /20050810/
    Publication Date: 2005-08-11
    Keywords: ddc: 610
    Language: English
    Type: conferenceObject
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  • 3
    ISSN: 1432-1076
    Keywords: Noradrenaline ; Adrenaline ; Hypoglycaemia ; Infants
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The response of the sympathoadrenal system to hypoglycaemia of different etiology was studied in seven infants, aged 10–189 days. Five infants had hyperinsulinism secondary to nesidioblastosis or to a β-cell adenoma of the pancreas, one infant had neonatal sepsis due to staphylococcal infection and one infant congenital growth hormone (HGH) and adrenocorticotropic hormone (ACTH) deficiency. In babies with hyperinsulinism, plasma noradrenaline increased from 0.29±0.03 to 0.61±0.09 ng/ml (P〈0.01), whereas adrenaline increased only in three, but did not change in two babies. Increases in heart rate and blood pressure paralleled these changes. In hypoglycaemia due to congenital sepsis, noradrenaline increased from 0.39 to 1.64 ng/ml and adrenaline from 0.05 to 0.86 ng/ml. This was associated with marked haemodynamic changes. In congenital HGH and ACTH deficiency, the low basal plasma levels of noradrenaline (0.12 ng/ml) and adrenaline (0.01 ng/ml) remained unchanged in response to hypoglycaemia. Heart rate and blood pressure were unaffected. The sympathoadrenal system was activated by hypoglycaemia in all infants except in congenital HGH and ACTH deficiency. In contrast to adults, noradrenaline was the preferentially released catecholamine, suggesting an involvement of noradrenaline in glucose counter regulation in infancy.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1432-1041
    Keywords: stress ; plasma catecholamines ; beta-blockade ; hemodynamic effects
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Summary The effect of calculation stress on hemodynamic parameters and plasma adrenalin and noradrenalin was studied in two groups of 6 male subjects, before and duringβ-Blockade. One group received propranolol 15 mg i. v. and the other received mepindolol sulphate 0,5 mg i. v. There was an increase in heart rate, cardiac output and blood pressure during mental stress. A significant increase in plasma adrenalin but not in noradrenalin occurred at the same time. The stress-induced rise in HR but not that in blood pressure could be prevented byβ-receptor blockade with proprandolol and mepindolol sulfate. The peripheral resistance (PR) and diastolic blood pressure in stress were even higher after propranolol than in the control study. Propranolol had no effect on the increased adrenalin concentration during stress, but it was prevented by mepindolol sulfate. There was no correlation between the increase in HR and that in adrenalin during stress, but the HR in stress and the HR reaction to infused isoproterenol were highly correlated.
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1432-1041
    Keywords: diltiazem ; verapamil ; calcium antagonists ; angiotensin II ; plasma catecholamines ; hypotensive effects
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Summary To evaluate the possible functional antagonism of the calcium antagonists diltiazem and verapamil of the sympathetic nervous system and the renin-angiotensin system, their influence on blood pressure, heart rate, plasma catecholamines and renin activity (PRA), and on the reaction of these parameters to exogenous noradrenaline (NA) and angiotensin II, was investigated in 8 normotensive volunteers. Intravenous diltiazem or verapamil caused a sharp, shortlasting decrease in systolic and diastolic blood pressure, with a maximum 1–3 min after injection and a duration of 10–15 min. Even a further infusion of the calcium antagonists was unable to maintain the initial hypotensive effect. The cessation of the hypotensive effect was not due to reflex stimulation of the sympathetic nervous system, as indicated by unchanged plasma NA and adrenaline levels in the case of diltiazem, but was associated with an increase in PRA. During the administration of diltiazem and verapamil, the increase in blood pressure in response to the infusion of NA and angiotensin II was attenuated; the increase in diastolic pressure was mainly affected. The inhibition was more pronounced at the higher infusion rate of NA and angiotensin II. On the basis of these findings it is suggest that the hypotensive activity of calcium antagonists can be at least partly attributed to a reduction in vascular tone which is maintained by the postjunctional action of noradrenaline and angiotensin II.
    Type of Medium: Electronic Resource
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  • 6
    ISSN: 1435-0130
    Keywords: Catecholamines ; Burns ; Anaesthesia ; Operative treatment
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The plasma levels of adrenaline and noradrenaline were determined by a radioenzymatic method in 6 severely burned patients during the course of treatment and during the surgical procedures. The mean level of noradrenaline of all patients was 0.83±0.48 ng/ml during the first week of treatment, 0.62±0.40 ng/ml during the 2nd week and 0.61±0.42 ng/ml during the 3rd week. The corresponding levels of adrenaline were 0.23±0.20 ng/ml, 0.13±0.08 and 0.08±0.04 ng/ml, respectively. — These levels of catecholamines were lower than those reported in literature. However the surgical treatment provoked a considerable increase of especially noradrenaline intra-as well as postoperatively. This increase was most pronounced during the first operation performed within the 3rd and 13th day after the thermal injury and was independent of the anaesthetic agent used. — The data indicate that adequate infusion, intensive care, warm environment (30–32 °C) and early surgical treatment are important factors in the treatment of burn patients. Additionally warm environment during operation and short operation time are considered to be beneficial.
    Type of Medium: Electronic Resource
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  • 7
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 8
    ISSN: 1365-2826
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: In situ hybridization was used to study the mRNA levels for secretogranin II and VGF in comparison with those of oxytocin and vasopressin in the hypothalamus of rats. VGF is a widespread constituent of large dense core vesicles which is selectively induced in PC12 cells by nerve growth factor. After adrenalectomy the mRNA levels of secretogranin II, VGF and vasopressin were increased 4- to 5-fold in the parvocellular neurons of the paraventricular nuclei. In lactating rats the message for oxytocin and secretogranin II were significantly elevated in the magnocellular neurons of the paraventricular and supraoptic nuclei, whereas for VGF only a smaller non-significant increase was observed. As shown by immunoelectron microscopy secretoneurin (a peptide derived from secretogranin II) and oxytocin are co-stored in the large dense core vesicles of the hypothalamo-neurohypophysial neurons.These results demonstrate that stimulation of both parvo- and magnocellular neurons of the hypothalamus induces a concomitant increase of the messages for secretogranin II and VGF together with those of vasopressin and oxytocin.
    Type of Medium: Electronic Resource
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  • 9
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 10
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Serotonergic neurones are among the first to develop in the central nervous system. Their survival and maturation is promoted by a variety of factors, including serotonin itself, brain-derived neurotrophic factor (BDNF) and S100β, an astrocyte-specific Ca2+ binding protein. Here, we used BDNF-deficient mice and cell cultures of embryonic raphe neurones to determine whether or not BDNF effects on developing serotonergic raphe neurones are influenced by its action on glial cells. In BDNF–/– mice, the number of serotonin-immunoreactive neuronal somata, the amount of the serotonin transporter, the serotonin content in the striatum and the hippocampus, and the content of 5-hydroxyindoleacetic acid in all brain regions analysed were increased. By contrast, reduced immunoreactivity was found for myelin basic protein (MBP) in all brain areas including the raphe and its target region, the hippocampus. Exogenously applied BDNF increased the number of MBP-immunopositive cells in the respective culture systems. The raphe area displayed selectively reduced immunoreactivity for S100β. Accordingly, S100β was increased in primary cultures of pure astrocytes by exogenous BDNF. In glia-free neuronal cultures prepared from the embryonic mouse raphe, addition of BDNF supported the survival of serotonergic neurones and increased the number of axon collaterals and primary dendrites. The latter effect was inhibited by the simultaneous addition of S100β. These results suggest that the presence of BDNF is not a requirement for the survival and maturation of serotonergic neurones in vivo. BDNF is, however, required for the local expression of S100β and production of MBP. Therefore BDNF might indirectly influence the development of the serotonergic system by stimulating the expression of S100β in astrocytes and the production MBP in oligodendrocytes.
    Type of Medium: Electronic Resource
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