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  • 1990-1994  (941)
  • 1950-1954  (139)
  • 1880-1889  (15)
  • 1850-1859  (1)
  • 1
    Electronic Resource
    Electronic Resource
    s.l. : American Chemical Society
    Analytical chemistry 64 (1992), S. 3202-3205 
    ISSN: 1520-6882
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1520-6882
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    s.l. : American Chemical Society
    Journal of agricultural and food chemistry 42 (1994), S. 2099-2107 
    ISSN: 1520-5118
    Source: ACS Legacy Archives
    Topics: Agriculture, Forestry, Horticulture, Fishery, Domestic Science, Nutrition , Process Engineering, Biotechnology, Nutrition Technology
    Type of Medium: Electronic Resource
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  • 4
    Publication Date: 2021-03-16
    Language: English
    Type: article , doc-type:article
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  • 5
    ISSN: 1471-0528
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Objective To determine whether there is a dose-iresponse effect of percutaneous oestradiol implants on the skeletons of postmenopausal women using a range of doses available in clinical practice.Design One year randomised study.Subjects Forty-five postmenopausal women who requested oestrogen replacement therapy were randomised to receive 25 mg, 50 mg, or 75 mg oestradiol implants. The bone mineral density changes were compared with a control group of 15 untreated women.Main outcome measures Dual energy X-ray absorptiometry using Hologic 1000 QDR before treatment and after one year of treatment. Plasma oestradiol and follicle stimulating hormone levels before treatment and after one year.Results There were significant correlations between the plasma oestradiol levels and the percentage increase in bone density at the lumbar spine, the total hip, the femoral neck, and the trochanter. The median (range) plasma oestradiol level was 327 pmol/1 (114–853) in the 25 mg group, 358 pmol/1 (220–957) in the 50 mg group and 518 pmol/1 (167–828) in the 75 mg group. Three women who lost a significant amount of bone from the clinically relevant sites in the 25 mg oestradiol group all had plasma oestradiol levels below 300 pmol/1. None of the women in either the 50 mg or 75 mg oestradiol groups lost bone from these sites.Conclusions Oestradiol implants resulted in a wide range of circulating oestradiol levels with each of the doses used. There was a significant relation between plasma oestradiol levels and the increases in bone density at both the lumbar spine and the proximal femur. None of the women lost bone density at the clinically important sites of the spine and femoral neck if their plasma oestradiol levels were above 300 pmol/1.
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    BJOG 101 (1994), S. 0 
    ISSN: 1471-0528
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 7
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 61 (1993), S. 0 
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: A peptidylarginine deiminase (PAD; EC 3.5.3.15) has been isolated from bovine brain and some of its characteristics have been studied. The enzyme showed an absolute requirement for Ca2+, a temperature optimum at ∼50°C, and two Kmvalues when benzoylarginine ethyl ester was used as substrate, 0.78 mMand 11.2 mM.The higher Kmhas not been reported previously. Protein substrates for the enzyme included polyarginine and myelin basic protein but not histones. Because one of the components of MBP contains six citrullinyl residues per mole, enzymic deimination appeared to be a likely mechanism. When the most cationic component (C-1) was subjected to PAD in solution, 17 of the 19 arginyl residues were modified. From sequence analyses we concluded that the nature of the amino acid residues adjacent to the deiminated arginine were not modifiers of the reaction as arginyl residues in a variety of environments were deiminated. This deimination was reflected in a large increase in random structure, as measured by [θ]200. At 5°C, the [θ]200of the deiminated protein was -70 × 103 compared with -30 × 103 deg cm2/dmol for the native protein. When the temperature was increased to 70°C, the [θ]200 was -44 × 103 for the deiminated protein and -20 × 107 deg cm2/ dmol for the native C-1. When plotted as a function of temperature, [θ]200 decreased linearly from 5°C to 50°C for both proteins and did not change from 50°C to 70°C. PAD provides a mechanism for deimination of arginyl residues of myelin basic protein. The selective deimination of the six arginyl residues that are consistently found deiminated in C-8 may be determined by the orientation of the protein in the membrane and/or the more complex lipid composition of myelin may affect the selectivity of the deimination.
    Type of Medium: Electronic Resource
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  • 8
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 60 (1993), S. 0 
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Human tyrosine hydroxylase (HTH) RNA undergoes alternative splicing, and four different forms of HTH mRNA have been previously identified. Rabbit antibodies were raised against octapeptides unique to each of the four isoforms of HTH predicted from these mRNAs. Blot immunolabeling of human adrenal medulla, pheochromocytoma, and several neuroblastoma cell lines with affinitypurified anti-HTH peptide antibodies demonstrated the presence of all four HTH isoforms in each of these tissues. Quantitative immunolabeling assays for HTH-1, -2, and -4 were established, and HTH isoform levels were determined in several human neuroblastoma cell lines. Whereas total HTH levels differed up to fourfold among the HTH-positive neuroblastoma cell lines studied [LA-N-1, LA-N-5, CHP-234, BE(2)-C, and BE(2)-M17], the relative abundances of HTH isoforms in each of the cell lines were similar. Immunocytochemical analyses demonstrated that HTH immunoreactivity was distributed unequally among the cells in each of these neuroblastoma lines, and morphological interconversion did not account for this heterogeneity. A direct relationship between the percentage of HTH-positive cells and overall HTH levels was also observed. This relationship, in the absence of an apparent clonal basis for the heterogeneity, suggests that HTH expression in neuroblastoma cells may be controlled in a relatively “all-ornone”(bimodal) fashion.
    Type of Medium: Electronic Resource
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  • 9
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: This study explored further the function of the metabotropic excitatory amino acid receptor in the rat brain. The trans and cis isomers of (±)-1-amino-1,3-cyclopentane-dicarboxylic acid (ACPD) were characterized for relative affinities at ionotropic and metabotropic excitatory amino acid receptors in vitro, as well as ability to produce in vivo excitatory or excitotoxic effects in rats. trans-ACPD was about 12 times more potent in vitro as an agonist for metabotropic excitatory amino acid receptors when compared to its ability to displace N-methyl-D-aspartate (NMDA) ([3H]CGS-19755) receptor binding. cis-ACPD was about 30 times more potent as a displacer of [3H]CGS-19755 binding than as a stimulant of phosphoinositide hydrolysis. When administered intra-peritoneally to neonatal rats, both cis- and trans-ACPD produced convulsions that were prevented by the competitive NMDA receptor antagonists, LY233053 and LY274614. cis-ACPD was six times more potent as a convulsant when compared to trans-ACPD. Both compounds were examined for excitotoxic effects in vivo following stereotaxic injection into the mature or neonatal rat striatum. Doses of trans-ACPD of up to 5,000 or 1,200 nmol produced few signs of striatal neuronal degeneration in the mature or neonatal brain, respectively. However, cis-ACPD produced extensive dose-related neuronal degeneration at doses of 100–1,000 nmol in the mature brain and 50–200 nmol in the neonatal brain. These studies suggest that, unlike the ionotropic excitatory amino acid receptors, activation of the metabotropic excitatory amino acid receptor does not result directly in excitatory effects, such as excitotoxicity.
    Type of Medium: Electronic Resource
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  • 10
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 56 (1991), S. 0 
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: In immature rodent brain, the glutamate receptor agonist N-methyl-D-aspartate (NMDA) is a potent neurotoxin. In postnatal day (PND)-7 rats, intrastriatal injection of 25 nmol of NMDA results in extensive ipsilateral forebrain injury. In this study, we examined alterations in high-affinity [3H]glutamate uptake (HAGU) in NMDA-lesioned striatum. HAGU was assayed in synaptosomes, prepared from lesioned striatum, the corresponding contralateral striatum, or unlesioned controls. Twenty-four hours after NMDA injection (25 nmol), HAGU declined 44 ± 8% in lesioned tissue, compared with the contralateral striatum (mean ± SEM, n = 6 assays, p 〈 0.006, paired t test). Doses of 5–25 nmol of NMDA resulted in increasing suppression of HAGU (5 nmol, n = 3; 12.5 nmol, n = 3; and 25 nmol, n = 5 assays; p 〈 0.01, regression analysis). The temporal evolution of HAGU suppression was biphasic. There was an early transient suppression of HAGU (−28 ± 4% at 1 h; p 〈 0.03, analysis of variance, comparing changes at 0.5, 1, 2, and 3 h after lesioning); 1 or 5 days postinjury there was sustained loss of HAGU (at 5 days, −56 ± 11%, n = 3, p 〈 0.03, paired t test, lesioned versus contralateral striata). Treatment with the noncompetitive NMDA antagonist MK-801 (1 mg/kg i.p.) attenuated both the early and subsequent irreversible suppression of HAGU (1 h postlesion −28 ± 4%, n = 6 assays versus −12.6 ± 5% with MK-801, n = 4, p= 0.005; 24 h postlesion, −44 ± 8%, n = 5, versus +2.4 ± 6%, n = 3 with MK-801, p= 0.01, Wilcoxon ranked sum tests). In immature brain excitotoxic lesions produce an acute reversible suppression of HAGU, and a delayed long-lasting reduction in HAGU secondary to brain injury. These data suggest that accumulation of endogenous glutamate, as a consequence of the acute disruption of HAGU, could contribute to the pathogenesis of excitotoxic neuronal injury.
    Type of Medium: Electronic Resource
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